Kusetuskampanjan sisältö on ollut, että korona-virusryhmän ikiaikaisia, laajalle jakautuneita ominaisuuksia esitetään muka "mahdollisiksi syntyä vain laboratorio-olosuhteissa"...
Aivopierun lähettivät liikkeelle kaksi NATO:n-Bilderbergin-WEF:n infosoturia, (vale-)AIDS-rototetutkijat britti Angus Dalgleish ja norjalainen Birger Sørensen
Molemmat nämä herrat tekivät muuten "Halosen-Rissalan-ihmepelastuksen" vuonna 2014 Ukrainan sotatoimialueen yläpuolella (jonne ei missään tapauksessa olisi saa-nut matkustajakoneella lentää!) alasammutun Malaysian Airlinesin MH17-matkusta-jakoneen matkasta, jossa oli menossa EU-maiden delegaatio Melbournen AIDS-rokote-maailmankonferenssiin.
Onnettomuudessa kuoli 6 EU:n johtavaa (parhaiten rahoitettua, paitsi Dalgleish ja Sørensen ja Pekka Sillanaukee, €100 mlj.) AIDS-rokotetutkijaa mukaan lukien alan maailmanjärjestön ja Melbornen konferenssin hollantilainen puheenjohtaja Joep Lange ja lisäksi parikymmentä heidän assistenttiaan, sihteeriään ja perheenjäsentään. Rokotetta ei ole vieläkään - ja tuskin koskaan tuleekaan.
https://tekniikanmaailma.fi/koronavirus-lahti-todennakoisesti-liikkeelle-laboratoriosta-usan-energiaministerio-uskoo-nyt-tiedustelujarjestot-ovat-erimielisia-asiasta/
" Tiede Lääketiede
|27.2.2023 6:10
Koronavirus lähti todennäköisesti liikkeelle laboratoriosta, USA:n energiaministeriö uskoo nyt – Tiedustelujärjestöt ovat erimielisiä asiasta

Koronaviruksen omikronmuunnos.
Istock
***
Keskustelua:
Risto Koivula
23.05.2021 09:55:33
405355
Re: Pääministeri Marinkin myöntää koronapandemian olleen keinotekoinen
Lainaus: Teppolainen, 20.05.2021 15:57:34, 405340
Se vaan ei ole keinotekoinen, eikä Marinkaan tuossa sellaista väitä. Se ei myskään "johdu 1000-vuotisesta patriakaatista"...
YK:n (EU-pölkky)pääsihteeri Guterrez:
"Koronavirus on 1000-vuotisen PATRIARKAATIN SYYTÄ!!!"
https://russian.rt.com/inotv/2020-09-08/Daily-Mail-gensek-OON-vozmutil
" Daily Mail: генсек ООН возмутил соцсети, связав пандемию с «тысячелетием патриархата»
Оригинал новости ИноТВ:
Daily Mail: генсек ООН возмутил соцсети, связав пандемию с «тысячелетием патриархата»
Оригинал новости ИноТВ:
В интернете распространяются призывы лишить ООН финансирования. Пово-дом для недовольства стало заявление главы международной организации о том, что пандемия коронавируса — «демонстрация патриархата», пишет Daily Mail.
Internetissä leviää vaatimus alentaa YK:n rahoitusta. Tyytymättömyyden lähde on kansainvälisen organisaation johtajan tiedotus siitä, että koronsaviruspandemia oa "patriarkaatin demonstraatio", kirjoittaa Daily Mail.
Facebook KIELTÄYTYI JULKASEMASTA TÄTÄ!!! "

Teppolainen
24.05.2021 11:41:18
405357
WSJ: Laboratoriossa joutui useita henkilöitä sairaalahoitoon COVID-19 taudin oireiden vuoksi ennen pandemian alkua
Yhdysvaltain mukaan useita henkilöitä sairastui Wuhanin viruslaboratoriossa mystisesti Covid19 taudin oireisiin ja joutui sairaalaan:
https://www.wsj.com/articles/intelligence-on-sick-staff-at-wuhan-lab-fuels-debate-on-covid-19-origin-11621796228
Myöskään Kiina ei suostu jutun mukaan avaamaan tietoja laboratoriossa tutkituista viruksista, jotta vaihtoehto laboratoriosta lähteneestä viruksesta voitaisiin poissulkea.
Se että tutkijoiden mukaan viruksen genomia ole tarkoituksellisesti muunneltu laboratoriossa, ei vielä tarkoita etteikö se olisi silti voinut olla lähtöisin laboratorio-olosuhteista.
...
Uusi tutkimus on julkaisemassa todisteita, joiden mukaan Covid olisi kiinalaisten tarkoituksella luoma virus, jonka jälkiä olisi peitelty muuntamalla virusta luonnollisemman oloiseksi:
https://www.foxnews.com/world/explosive-study-claims-to-prove-chinese-scientists-created-covid
" Coronavirus
Published May 29, 2021 2:29pm EDT
Explosive study claims to prove Chinese scientists created COVID
British Professor Angus Dalgleish and Norwegian scientist Dr. Birger Sørensen wrote they’ve had primary evidence 'of retro-engineering in China'
A bombshell new study claims to have proof that Chinese scientists created COVID- 19 in a lab and then tried to reverse-engineer versions of the virus to make it look like it evolved naturally from bats.
British Professor Angus Dalgleish and Norwegian scientist Dr.Birger Sørensen wrote they’ve had primary evidence "of retro-engineering in China" since last year,but were ignored by academics and major medical journals, The Daily Mail reported Saturday, citing the soon-to-be-published study.
The study concludes: "the likelihood of it being the result of natural processes is very small." The virus is still killing 12,000 people a day around the world.
POMPEO SAYS WUHAN LAB WAS ENGAGED IN MILITARY ACTIVITY ALONGISDE CIVILIAN RESEARCH
Dalgleish is a London oncology professor known for breakthrough work on a vaccine for HIV. Sørensen is a virologist and chair of the pharmaceutical company Immunor, which developed a coronavirus vaccine candidate called Biovacc-19. Dalgleish also has a financial stake in that company.
It was during their COVID-19 vaccine research that the pair came across "unique fin-gerprints" indicating the virus didn’t come from nature, they said. The telltale clue: a rare finding in the COVID-carrying virus of a row of four amino acids, which give off a positive charge and bond to negative human cells.
INTEL COMMUNITY ‘AGGRESSIVELY’ INVESTIGATING COVID-19 ORIGIN
"The laws of physics mean that you cannot have four positively charged amino acids in a row," Dalgleish told the Daily Mail. "The only way you can get this is if you artificially manufacture it."
They also tracked published Chinese research, some done working with American universities, to show how the tools to create the virus were allegedly built. A good part of the work reviewed involved "gain of function" research, which involves mani-pulating natural viruses in a lab to make them more infectious, allowing scientists to study their potential effect on humans.
The U.S. put a moratorium on such research in 2014. But it’s impossible to know if $600,000 funding for medical research in China was used for gain of function research, Dr. Anthony Fauci told Congress last week. "
[RJK: Absolute bullshit!]
Viruksen varjolla kiinalaiset onnistuivat kiristämään totalitarismia omassa maassaan ja edistämään totalitarismia myös ulkomailla, jopa Suomessa, samalla kun heikentävät kilpailijamaitaan taloudellisesti.
On yhä selvempää, että Marinin hysteerinen koronastrategia on ollut täysin virheelli-nen - ja ulkomailta johdetulle Marinille tarpeeton totalitarismin lisääminen ei selvästi-kään ole tuottanut omantunnon tuskia. Marin ei ole edes yrittänyt edistää painostus-toimia Kiinaa vastaan, jotta viruksen alkuperä olisi saatu tyrehdytettyä. Edes sitä Marin ei ole tehokkaasti pyrkinyt estämään, että virusta tulisi Suomeen kolmansien maiden kautta. Sen sijaan Marin keskittyy rajoittamaan mielenosoitusoikeutta ja kokoontumisvapautta, ikään kuin se olisi ollut tehokkain mahdollinen keino viruksen leviämisen ehkäisemisessä.
***
Teppolainen
30.05.2021 14:38:32
405405
Pääministeri Marinin koronahysteria on yhä naurunalaisempi ajautuessaan kompukseen Kiinan kanssa
Lainaus: PeP, 30.05.2021 14:15:29, 405404
Lainaus: Teppolainen, 30.05.2021 11:34:17, 405400
On yhä selvempää, että Marinin hysteerinen koronastrategia on ollut täysin virheellinen - ja ulkomailta johdetulle Marinille tarpeeton totalitarismin lisääminen ei selvästikään ole tuottanut omantunnon tuskia.
On yhä selvempää,että Suomen hallitus oli valinnut aivan oikean linjan koronan vas- tatoimissa. Hallitus kuunteli asiantuntijoita syyllistymättä ylilyönteihin ja kykeni nou-dattamaan tehokasta strategiaa koronan torjunnassa. Joistain virheistä huolimatta sekä sairastuvuus, että koronakuolleisuus ovat olleet Suomessa Euroopan alhaisim-pia. Samaan aikaan talouden notkahdus on ollut useita Euroopan maita pienempi. Hallitukselle voi antaa koronan hoitamisessa hyvän arvosanan kaikenkarvaisten salaliittoteoreetikkojen huuhailusta huolimatta.
Teppolainen: "Nämä mainitsemasi asiat tapahtuivat totalitaristi Marinin hallituksesta huolimatta, ei hysteerisen koronastrategian ansiosta.
On yhä selvempää, että Marinin kaltaisia hyypiöitä ajavat täysin muut asiat kuin ih-misten hyvinvointi, kokoontumisenvapaus, sananvapaus ja muut yleisesti arvostetut asiat."
Risto Koivula
30.05.2021 15:30:15
405406
Tavallisia koronavirusryhmän ominaisuuksia esitetään "mahdottomina muualla paitsi laboratoriossa"
Lainaus: Teppolainen, 30.05.2021 11:34:17, 405400
" Uusi tutkimus on julkaisemassa todisteita, joiden mukaan Covid olisi kiinalaisten tarkoituksella luoma virus, jonka jälkiä olisi peitelty muuntamalla virusta luonnollisemman oloiseksi:
https://www.foxnews.com/world/explosive-study-claims-to-prove-chinese-scientists-created-covid
Viruksen varjolla kiinalaiset onnistuivat kiristämään totalitarismia omassa maassaan ja edistämään totalitarismia myös ulkomailla, jopa Suomessa, samalla kun heikentävät kilpailijamaitaan taloudellisesti.
On yhä selvempää, että Marinin hysteerinen koronastrategia on ollut täysin virheelli-nen - ja ulkomailta johdetulle Marinille tarpeeton totalitarismin lisääminen ei selvästi-kään ole tuottanut omantunnon tuskia. Marin ei ole edes yrittänyt edistää painostus-toimia Kiinaa vastaan, jotta viruksen alkuperä olisi saatu tyrehdytettyä. Edes sitä Marin ei ole tehokkaasti pyrkinyt estämään, että virusta tulisi Suomeen kolmansien maiden kautta. Sen sijaan Marin keskittyy rajoittamaan mielenosoitusoikeutta ja kokoontumisvapautta, ikään kuin se olisi ollut tehokkain mahdollinen keino viruksen leviämisen ehkäisemisessä. "
Nuo tiedot ovat humpuukia, samoin nämä:
https://nypost.com/2021/05/29/explosive-study-claims-to-prove-chinese-scientists-created-covid/
Explosive study claims to prove Chinese scientists created COVID
By Eileen AJ Connelly
May 29, 2021
A bombshell new study claims to have proof that Chinese scientists created COVID- 19 in a lab and then tried to reverse-engineer versions of the virus to make it look like it evolved naturally from bats.
British professor Angus Dalgleish and Norwegian scientist Dr. Birger Sørensen wrote they’ve had primary evidence “of retro-engineering in China” since last year, but were ignored by academics and major medical journals, the Daily Mail reported Saturday, citing the soon-to-be-published study.
The study concludes: “the likelihood of it being the result of natural processes is very small.” The virus is still killing 12,000 people a day around the world.
Dalgleish is a London oncology professor known for breakthrough work on a vaccine for HIV. Sørensen is a virologist and chair of a pharmaceutical company, Immunor, which developed a coronavirus vaccine candidate called Biovacc-19. Dalgleish also has a financial stake in that company.
It was during their COVID-19 vaccine research that the pair came across “unique fin-gerprints” indicating the virus didn’t come from nature, they said. The telltale clue: a rare finding in the COVID-carrying virus of a row of four amino acids, which give off a positive charge and bond to negative human cells.
Some scientists believe the virus could have emanated from the Wuhan Institute of Virology in China.AFP via Getty Images
“The laws of physics mean that you cannot have four positively charged amino acids in a row,” Dalgleish told the Daily Mail. “The only way you can get this is if you artificially manufacture it.”
They also tracked published Chinese research, some done working with American universities,to show how the tools to create the virus were allegedly built.A good part of the work reviewed involved “gain of function” research, which involves manipula-ting natural viruses in a lab to make them more infectious,allowing scientists to study their potential effect on humans.
The US put a moratorium on such research in 2014. But it’s impossible to know if $600,000 in funding for medical research in China was used for gain of function research, Dr. Anthony Fauci told Congress last week.

British professor Angus Dalgleish (pictured) and Norwegian scientist Dr. Birger Sørensen claim to have proof COVID was created in a lab.
Chris Radburn/PA Wire/ZUMAPRESS.com
“A natural virus pandemic would be expected to mutate gradually and become more infectious but less pathogenic, which is what many expected with the COVID-19 pandemic but which does not appear to have happened,” the scientists wrote.
The scientists could not immediately be reached by The Post for comment.
News of the study comes amid renewed interest in COVID-19’s origins, which had long been proclaimed to have made the jump from bats to humans at a wet market in China. "
***
Marco Rubio Grills Fauci On Past Statements Of COVID-19 Origin
Sen. Rubio Grills Fauci: "Why Did You Dismiss The Lab-Leak Theory?"
https://www.facebook.com/SeanHannity/videos/476352046988364

***
Oikeat tiedot löytyvät täältä:
https://www.sciencedirect.com/science/article/pii/S1873506120304165
" Stem Cell Research
Volume 50, January 2021, 102115
Furin cleavage sites naturally occur in coronaviruses
Author links open overlay panel Yiran Wu a, Suwen Zhao b:
https://doi.org/10.1016/j.scr.2020.102115
Under a Creative Commons license
Highlights
• Phylogenetic tree of spike proteins reveals major groups of coronaviruses.
• Furin cleavage sites at spike S1/S2 are common in coronaviruses.
• Furin cleavage sites at spike S1/S2 naturally occurred independently for multiple times in coronaviruses.
Abstract
The spike protein is a focused target of COVID-19, a pandemic caused by SARS-CoV-2. A 12-nt insertion at S1/S2 in the spike coding sequence yields a furin clea-vage site, which raised controversy views on origin of the virus. Here we analyzed the phylogenetic relationships of coronavirus spike proteins and mapped furin recog-nition motif on the tree. Furin cleavage sites occurred independently for multiple times in the evolution of the coronavirus family, supporting the natural occurring hypothesis of SARS-CoV-2.

1. Introduction
The coronavirus disease 2019 (COVID-19) pandemic, caused by coronavirus SARS-CoV-2,is still rapidly spreading. Scientists all around the world are studying the infec- tion process of the virus and looking for therapeutic solutions to prevent and cure the disease. Spike protein is one of most important targets in COVID-19 research, not only in mechanism study but also in vaccine development and therapeutic antibody design (Premkumar et al., 2020, Abraham, 2020). The spike protein forms a homo-trimer (Fig. 1A) and protrudes outside the membrane of the virion (Li, 2016, Wrapp et al., 2020, Walls et al., 2020). It binds to angiotensin-converting enzyme 2 (ACE2) on human cell surface, undergoes conformational changes, and mediates the fusion of the virion to human cells (Li et al., 2003, Yan et al., 2020, Lan et al., 2020, Wang et al., 2020, Benton et al., 2020).

Fig. 1. Structure of SARS-CoV-2 spike protein (PDB ID: 6VYB (Walls et al., 2020). A) Spike homotrimer in open conformation. B) Cleavage sites on spike protein (marked by arrows). Red cartoon, S1; light/dark blue cartoon, S2; dark blue cartoon, S2′). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
The spike protein consists of two subunits: the N-terminal S1 subunit, containing the receptor binding domain that interacts with ACE2 and induces conformational change; while the C-terminal S2 subunit,containing the fusion peptide that is respon- sible for fusing the membranes of virion and human cells (Li, 2016). To function pro-perly, the spike protein needs to be cleaved by host proteases to separate the two subunits (Simmons et al., 2013). Study of SARS-CoV (caused the severe acute res-piratory syndrome in 2002-2003 and belonged to the same species as SARS-CoV-2) showed that cleavage at S1/S2 enhances fusogenicity of spike protein (Bosch et al., 2003). Another cleavage site producing S2′ (fusion peptide and the C-terminal region of S2) was also identified (Fig.1B) (Belouzard et al.,2009).The S2′ site is not far from the S1/S2 site, and cleavage either or both them can yield the separation of two sub-units of spike.For coronaviruses,multiple proteases were reported responsible for the cleavage, including TMPRSS2 (Hoffmann et al.,2020, Glowacka et al.,2011); cathep- sin CTSL (Bosch et al., 2008, Ou et al., 2020), and trypsin (Belouzard et al., 2009, Bertram et al., 2011).
The spike protein of the Middle East respiratory syndrome coronavirus (MERS-CoV) was discovered to be more effectively cleaved by another protease, furin (Millet and Whittaker, 2014). In MERS-CoV,both S1/S2 and S2′ sites have sequence RXXR, the furin recognition motif. In human body, furin is ubiquitously expressed (Braun and Sauter, 2019). This may explain the highly lethal nature and high rate of multiple system failure caused by MERS (Millet and Whittaker, 2014).
Surprisingly, SARS-CoV-2 has the furin recognition motif at S1/S2, causing by a 12-nucleotide insertion not presented even in its closest relatives (Walls et al., 2020, Coutard et al., 2020). This stimulates a conspiracy that this furin site can only be ma-nual work, thus SARS-CoV-2 must be created in a laboratory. Here, we analyzed the sequences of coronaviruses and found furin sites occurred independently for mul-tiple times during evolution. This exhibits natural occurrence of furin cleavage site in SARS-CoV-2 spike protein is highly possible. Thus, the insertion of furin cleavage site into SARS-CoV-2 spike protein is not necessarily a result of manual work.
2. Results
2.1. Phylogenetic tree of spike protein sequences reveals major groups of coronaviruses
Coronaviruses are members of the subfamily Orthocoronavinae (also named Coro-navinae) in the family Coronavidae. There are four genera: Alphacoronavirus, Beta-coronavirus, Gammacoronavirus, and Deltacoronavirus. The first two genera only in-fect mammals, while the last two primarily infect birds but also mammals (Cui et al., 2019). We collected sequences of coronavirus spike proteins from the InterPro data-base (Mitchell et al., 2019) and performed phylogenetic analysis. The phylogenetic tree (Fig. 2A) generally matches reported relationship of coronaviruses (Cui et al., 2019): three genera (Betacoronavirus; Gammacoronavirus, and Deltacoronavirus) each forms a single clade,while only Alphacoronavirus has a small group left outside (see Fig. 5 for representative sequences). The left-out Alphacoronavirus group con-tains Rhinolophus bat coronavirus HKU2 that was reported to be closely related to two typical Alphacoronavirus, human coronavirus NL63 and human coronavirus 229E, in a phylogenetic analysis based on the RNA-dependent RNA polymerase coding region (Cui et al., 2019). We aligned the whole genomes of the three viruses and found Rhinolophus bat coronavirus HKU2 is quite unique in its spike protein-coding region (Fig. S1). Such result explains why this clade was separated from other Alphacoronavirus in our phylogenetic analysis.

Fig. 2. Phylogenetic tree of coronavirus spike protein sequences. A) Noting genera of coronavirus. B) Subtree of Betacoronavirus, noting subgenera.
Furthermore, the five subgenera of Betacoronavirus were nicely displayed as mono-phyletic (Fig. 2B): Sarbecovirus (e.g. SARS-CoV-2 and SARS-CoV), Merbecovirus (e.g. MERS-CoV), Embecovirus (e.g. human coronavirus OC43 and human corona-virus HKU1, both causing common cold), and two small subgenera Hibecovirus and Nobecovirus. Hibecovirus and Nobecovirus are only discovered in bats so far, and our phylogenetic analysis shows they are related to Sarbecovirus.
2.2. Furin cleavage site at spike S1/S2 also occurs in a virus close to Sarbecovirus
We mapped the furin recognition motif RXXR at both S1/S2 and S2′ positions in phy-logenetic trees of spike protein sequences (Fig. 3, Fig. 4, Fig. 5 and S2, S3). In the Sarbecovirus + Hibecovirus + Nobecovirus clade (Fig. 3), furin cleavage sites at either position occur only in limited ranges. Strains of SARS-CoV-2 (we also added sequences from the GISAID database) have furin cleavage sites at spike S1/S2.
Moreover, SARS-CoV-2 is the only virus in subgenus Sarbecovirus having this feature, while even its closest relatives, bat coronavirus RaTG13 (sequence identity 97.7%) and pangolin coronaviruses (92.9%–90.7%), do not have furin site. However, in Hibecovirus, the sister clade of Sarbecovirus, a Hipposideros bat coronavirus col-lected in 2013 at Zhejiang Province in China has furin site at S1/S2. Interestingly, the other member in Hibecovirus lacks such site, similar to the situation of SARS-CoV-2 and its close relatives. The SARS-CoV-2 strains and Hipposideros bat coronavirus (Zhejiang 2013) are not sister groups, in agreement with the distinct sequence pat-terns of their furin cleavage sites at spike S1/S2 (Fig. 6A). Besides, two strains of bat coronavirus HKU9, belonging to Nobecovirus, are the only members in the Sarbeco-virus + Hibecovirus + Nobecovirus clade having furin cleavage site at spike S2′. ..."

Fig. 3. Mapping of furin recognition motif on phylogenetic tree of spike protein sequences, the Sarbecovirus + Hibecovirus + Nobecovirus clade. Sequences in the SARS-CoV-2 clade were clustered with 95% identity threshold; in the SARS-CoV-2 clade were clustered with 99% identity threshold.
Kuvasta ilmenee, että kyseinen "Furin cleavage sites -naula" tai "-piikki" esiintyy riippumattomasti coronavirusten evoluutiossa ja lisäksi ERI PAIKOISSA eri viruksilla. Kaikilla noilla viruksilla ei ole tekemistä ihmisen kanssa, joskin tuo ryhmä vaikuttaa olevan ihmiselle vaarallinen tarttuvuuden edistäjänä.
... Furin cleavage sites naturally occur in coronaviruses

Fig. 5. Mapping of furin recognition motif on phylogenetic tree of spike protein sequences, the Alphacoronavirus + Gammacoronavirus + Deltacoronavirus clade. Sequences clustered with 95% identity threshold.
Vastaava kartoitus Alphacoronavirus + Gammacoronavirus + Deltacoronavirus -tyypeillä.
" ... 2.2. Furin cleavage site at spike S1/S2 also occurs in a virus close to Sarbecovirus
We mapped the furin recognition motif RXXR at both S1/S2 and S2′ positions in phylogenetic trees of spike protein sequences (Fig. 3, Fig. 4, Fig. 5 and S2, S3). In the Sarbecovirus + Hibecovirus + Nobecovirus clade (Fig. 3), furin cleavage sites at either position occur only in limited ranges. Strains of SARS-CoV-2 (we also added sequences from the GISAID database) have furin cleavage sites at spike S1/S2.
Moreover, SARS-CoV-2 is the only virus in subgenus Sarbecovirus having this feature, while even its closest relatives, bat coronavirus RaTG13 (sequence identity 97.7%) and pangolin coronaviruses (92.9%–90.7%), do not have furin site. However, in Hibecovirus, the sister clade of Sarbecovirus, a Hipposideros bat coronavirus col-lected in 2013 at Zhejiang Province in China has furin site at S1/S2. Interestingly, the other member in Hibecovirus lacks such site, similar to the situation of SARS-CoV-2 and its close relatives. The SARS-CoV-2 strains and Hipposideros bat coronavirus (Zhejiang 2013) are not sister groups, in agreement with the distinct sequence pat-terns of their furin cleavage sites at spike S1/S2 (Fig. 6A). Besides, two strains of bat coronavirus HKU9, belonging to Nobecovirus, are the only members in the Sarbeco-virus + Hibecovirus + Nobecovirus clade having furin cleavage site at spike S2′.
2.3. Furin cleavage sites are common in Betacoronavirus
Our mapping results showed that the furin recognition motif is more common in Merbecovirus and Embecovirus (Figs. 4 and S2, S3). In Merbecovirus, furin sites at spike S1/S2 occur in three clades: MERS-CoV strains, the bat coronavirus HKU5 strains, and coronavirus Neoromicia/PML-PHE1/RSA/2011 with its relatives (Figs. 4A and S2). Besides, MERS-CoV and bat coronavirus HKU5 are the only clades in Merbecovirus having furin cleavage site at S2′.
In Embecovirus, furin recognition motif at spike S1/S2 is universal: All strains but a few exceptions have furin cleavage sites at spike S1/S2 (Figs. 4B and S3). Interes-tingly, the Longquan Aa mouse coronavirus (Wang et al., 2015) loses this furin site, while its close relatives (e.g. China Rattus coronavirus HKU24, sequence identity 96.0%) maintains the furin cleavage site. This provides an example of naturally oc-curred sequence variation at spike S1/S2 among closely related coronaviruses. Be-sides, for spike S2′, only several single strains have furin recognition motif (Fig. S3).
2.4. Furin cleavage sites also occur in other genera of coronavirus
Our mapping results showed furin cleavage sites are widely present in the whole co-ronavirus family (Fig. 5). For spike S1/S2, furin recognition motif is universal in Gam-macoronavirus, and also occurs in two clades of Alphacorovanvirus: feline coronavi-rus and relatives, and Chevrier's field mouse coronavirus. For spike S2′, furin recog-nition motif occurs in several independent clades, covering all the three genera. Notably, in the two human coronaviruses in Alphacoronavirus causing common cold, HCoV NL63 has furin cleavage site at spike S2′, while the HCoV 229E (protein sequence identity 63.8%) lacks such feature.
...

Fig. 6. Positions of furin cleavage sites at the linking region of S1 and S2. A) Multiple sequence alignment of representative Betacoronavirus spike protein S1/S2 region, with furin recognition motifs highlighted (red colorboxes in sequence alignment). Phylogenetic tree of spike protein se-quences is colored to indicate subgenera (coloring scheme the same as in Fig. 2B). B) Positions of furin cleavage sites in different coronavirus genera (red cartoon, furin recognition motif; red arrow, cleavage site); structures: SARS-CoV-2, PDB ID 6VYB (Walls et al., 2020), with missing loop added; feline coronavirus (FCoV) UU16, homology model based on PDB ID 5SZS (Walls et al., 2016); infectious bronchitis coronavirus (IBV), PDB ID 6CV0 (Shang et al., 2018). (For inter-pretation of the references to colour in this figure legend,the reader is referred to the web version of this article.)
2.5. Furin cleavages sites occurred independently for six times in Betacoronavirus
The alignment of linking regions of spike S1 and S2 domains in representative Betacoronavirus (Fig. 6A) shows this region is less conserved than the neighboring folded S1 and S2 segments. Within a subgenus the sequences are well aligned, but among subgenera the similarity is low. The furin cleavage site of SARS-CoV-2 spike S1/S2 is formed by a insertion of PRRA in comparison to other Sarbecovirus inclu-ding close relative RaTG13, showing it occurred very recently and independently. Si-milarly, Hipposideros bat coronavirus (Zhejiang 2013) in Hibecovirus has furin site of independent origin, though the occurring time is hard to decide for in this subgenera only two sequences were published.
Merbecovirus and Embecovirus both have multiple coronavirus species with furin cleavage sites at spike S1/S2, but their situations are different: In Merbecovirus, furin cleavage sites prevail in three non-sister clades (Figs. 4A and 6A). Moreover, the positions of furin recognition motifs in the linking regions are unique to each clade, as exhibited in alignments of both protein sequences (Fig. 6A) and nucleotide sequences (Fig. S4A). These indicated for of the three clades in Merbecovirus, furin cleavage sites have an independent origin. In Embecovirus, to the contrast, all the furin cleavage sites are variations based on a 5-residue region with consensus se-quence RRXRR. The region is well aligned in both protein and nucleotide sequences (Figs. 6A and S4B). This suggested the furin cleavage sites of Embecovirus share a common ancestor.
In addition, in Alphacoronavirus and Gammacoronavirus, S1/S2 cleavage sites re-side at a different loop comparing to the site in Betacoronavirus (Fig. 6B), therefore furin cleavage sites at spike S1/S2 in these two genera occurred independently from those in Betacoronavirus in evolution.
3. Discussion
Furin cleavage is critical to many viral diseases, including HIV, Ebola, and influenza H5 and H7 (Becker et al.,2012).Furin is a ubiquitously expressed protease.In human body, it has a wider distribution range than the major protease responsible for clea-ving spike, TMPRSS2 (Fig. S5). Therefore, coronaviruses with spike containing furin cleavage site may have advantage in spreading. Deletions of furin cleavage site in SARS-CoV-2 attenuates replication on respiratory cells (Johnson et al., 2020) and pathogenesis in hamster (Johnson et al.,2020, Lau et al., 2020). Furin inhibitors sup- press virus production and cytopathic effects in kidney cells (Cheng et al., 2020).
Natural polymorphisms losing furin recognition motif in SARS-CoV-2 spike S1/S2 are observed, but very rare (Xing et al.,2020). Variations in this region are more common in viruses cultured in vitro than viruses isolated from clinical samples, suggesting this cleavage site is under selection pressure in human body (Lau et al., 2020, Liu et al., 2020).
Our analysis exhibits furin cleavage sites at spike S1/S2 occurred independently for several times in coronavirus. Consequently, natural occurring of the site in SARS-CoV-2 is highly possible. This is further supported by other observed natural variations at the linking region of S1 and S2: A natural insertion in SARS-CoV spike though not related to furin recognition motif was reported (Zhou et al., 2020). In Embecovirus; Longquan Aa mouse coronavirus (Wang et al., 2015) has a frameshift mutation led to the loss of furin recognition motif (Fig. S4B); Some strains of murine coronavirus lose furin recognition motif through substitution mutations (Fig. S3), e.g. in MHV-2 (Yamada et al., 1997). Further study of losing the furin cleavage site in Embecovirus would help to interpret the S1/S2 cleavage of Betacoronaviruses.
Besides, independent occurrences of furin cleavage sites in surface glycoproteins are not unique to coronavirus: for the hemagglutinin of influenza, only H5 and H7 have furin cleavage sites (Bottcher-Friebertshauser et al., 2013); and these subtypes are distant in phylogenetic tree (Fig. S6). "
Risto Koivula
01.06.2021 09:53:48
405430
Pääministeri Marinin koronahysteria on yhä naurunalaisempi ajautuessaan kompukseen Kiinan kanssa
Lainaus: Teppolainen, 31.05.2021 12:49:05, 405416
Lainaus: PeP, 30.05.2021 14:15:29, 405404
Lainaus: Teppolainen, 30.05.2021 11:34:17, 405400
T: On yhä selvempää, että Marinin hysteerinen koronastrategia on ollut täysin virheellinen - ja ulkomailta johdetulle Marinille tarpeeton totalitarismin lisääminen ei selvästikään ole tuottanut omantunnon tuskia.
P: On yhä selvempää, että Suomen hallitus oli valinnut aivan oikean linjan koronan vastatoimissa. Hallitus kuunteli asiantuntijoita syyllistymättä ylilyönteihin ja kykeni noudattamaan tehokasta strategiaa koronan torjunnassa. Joistain virheistä huolimat-ta sekä sairastuvuus, että koronakuolleisuus ovat olleet Suomessa Euroopan alhai-simpia. Samaan aikaan talouden notkahdus on ollut useita Euroopan maita pienem-pi. Hallitukselle voi antaa koronan hoitamisessa hyvän arvosanan kaikenkarvaisten salaliittoteoreetikkojen huuhailusta huolimatta.
T: Kyse ei ole siitä etteikö myös jonkinlaisia rajoituksia olisi tarvittu, mutta rajoitusten priorisoiminen ja toteutustapa muutoinkin on sellainen, jolla ei ole mitään tekemistä koronaviruksen leviämisen kanssa, mutta sitäkin enemmän tekemistä totalitarismin ja kansalaisten kyykyttämisen kanssa.
Jokaiselle tulee elävässä elämässä vastaan tilanteita, jossa rajoitukset on toteutettu äärimmäisellä epäjohdonmukaisuudella;yhtä asiaa yhteiskunnallisesti rajoitetaan sa- malla kun jotain verrattain turhaa ja taloudellisesti vähän tuottavaa asiaa ei rajoiteta lainkaan, vaikka vaikutukset olisivat koronaviruksen leviämisessä samat.
Monelle tulee myös elävässä elämässä vastaan tilanteita, joissa ei millään tavoin edes perustoimeentulon tasoisesti kompensoida tilanteen aiheuttamia äärimmäisiä ongelmia samalla kun toimeentulotukea syydetään vapautuneesti niille joilla ei en-nestäänkään ole ollut mitään menetettävää eli rehelliset työtä tekevät kansalaiset lai-tetaan näkemään nälkää (vaikka ei olisi edes tosiasiallisesti omaa myytävää omai-suutta) samalla kun katuojassa makaaville juopoille syötetään entistä enemmän seteleitä pullasorsien tavoin.
Samaan aikaan perusoikeuksien ytimeen kuuluvia asioita rajoitetaan ilman omantunnontuskia samalla kun lasketaan punainen matto ulkomailta saapuvien tuontiviruslevittäjien eteen.
Tämä kaikki kertoo siitä, että on todella työskennelty olan takaa sen eteen, että totalitarismin edistämiselle löydettäisiin tekosyitä koronaviruksen varjolla.
RK: Mitä se "totilateralismi" on?
Paikkansa pitävää kiinalaista tiedettä?
Risto Koivula
01.06.2021 22:41:30
405437
Re: Tavallisia koronavirusryhmän ominaisuuksia esitetään "mahdottomina muualla paitsi laboratoriossa"
https://www.presstv.ir/Detail/2021/06/01/658013/www.presstv.ir
China blasts probe into COVID origin; warns US ‘could meet its Waterloo’
Tuesday, 01 June 2021 3:38 PM

Security personnel stand guard outside the Wuhan Institute of Virology in Wuhan as members of the World Health Organization team investigating the origins of the Covid-19 pandemic visit the institute in Wuhan in China's central Hubei province February 3, 2021. (Photo by AFP)
China has lambasted a newly-announced probe by the administration of US President Joe Biden whether the deadly coronavirus escaped from a laboratory in the Chinese city of Wuhan, warning that Washington “could meet its Waterloo in this battle.”
China's Global Times daily made the warning in an article published on Sunday and said the Biden administration was taking a “dangerous stance” by calling for a full investigation into the origins of the coronavirus pandemic.
Biden ordered US intelligence officials last week to “redouble” their efforts to investigate the pandemic's beginnings and determine whether it came from a lab accident in Wuhan or emerged from human contact with an infected animal.
He directed US national laboratories to assist with the investigation and the intelligence community to prepare a list of specific queries for the Chinese government.
Biden called on US intelligence agencies to report back within 90 days.

US senators seek probe into COVID-19 origins, accuse China of ‘cover-up’
The US Senate has passed a resolution calling for a probe into the origins of the coronavirus pandemic and senators accused Beijing of “cover-up”.
The Chinese paper said the investigation by US intelligence officials was entirely political and predicted that the team would likely “produce a slanderous report that is in line with the US' anti-China campaign.”
The state-owned newspaper called the US government “full of arrogance” for disres-pecting a previous report issued by an expert group of the World Health Organiza-tion (WHO), which conclude after its mission to Wuhan in late January that the coro-navirus outbreak was not likely to have been caused by a leak from the lab in the Chinese city, and that the virus was most probably transmitted to humans from bats via an intermediary animal.
“Washington is too arrogant to realize that its vicious accusations against China have become a political gamble for itself,” the article added. “The US could meet its Waterloo in this battle” by abusing its soft power to an extent that it would lose all credibility.
Virus likely jumped to humans from bats through 'missing link' animal: WHO report

Virus likely jumped to humans from bats through 'missing link' animal: WHO report
An international expert mission to Wuhan says it was very likely that COVID-19 first passed to humans from a bat through an intermediary animal.
The Chinese paper compared the virus probe with US efforts to find Weapons of Mass Destruction (WMD) in Iraq and also stressed that the US had placed itself in a “dangerous status.”
The article pointed out that Washington was totally wrong on the issue of WMD in the early 2000s and the invasion of Iraq on that pretext, insisting that US leaders “have lost their credibility at the very beginning of this race.”
“It will be difficult for the US to do what it did 18 years ago when Washington fabricated evidence of Iraq possessing WMDs to fool the international community,” the Chinese daily said.
“So far,the US intelligence agencies can ask only the US media to help spread those rumors anonymously because they do not have any real proof that can be shared with the whole world. This traditional strategy of a frame-up is powerless in today's environment.”
Meanwhile, Zhao Lijian,a Chinese foreign ministry spokesperson, said last week that Biden was not interested in “serious” scientific origin tracing and did not care about “facts or truth.”
Zhao also called on Washington to open up its own labs for investigation.
Biden ‘does not care about facts and truth’ about coronavirus: China
US President Joe Biden is playing politics by calling for an investigation into the origins of the coronavirus, the Chinese government has said.
The theory that the contagion had leaked from the Chinese lab was originally hyped up by, among others, the administration of former US president Donald Trump as part of his hawkish anti-China policies.
Since infecting its first victims in the central Chinese city of Wuhan in late 2019, the pandemic has spread to nearly every country across the globe, killing more than 3.4 million people so far.
China also called on the US to give a full clarification on its bio-military activities at home and abroad, a matter of concern shared by Russia and others. "
WHO on se, joka alkuperän mahdollisen epäilyttävyyden selvittää tieteellisin perustein.
https://www.presstv.ir/Detail/2020/05/04/624619/WHO-says-got-no-proof-from-US-on-'speculative'-Wuhan-lab-virus-claims
" WHO says virus 'natural in origin', and 'will be with us for a long time'
Monday, 04 May 2020 10:43 PM

The World Health Organization said Monday that Washington had provided no evidence to support "speculative" claims by the US president that the new coronavirus originated in a Chinese lab.
"We have not received any data or specific evidence from the United States government relating to the purported origin of the virus -- so from our perspective, this remains speculative," WHO emergencies director Michael Ryan told a virtual briefing.
Scientists believe the killer virus jumped from animals to humans, emerging in China late last year, possibly from a market in Wuhan selling exotic animals for meat.
But US President Donald Trump, increasingly critical of China's management of the first outbreak, claims to have proof it started in a Wuhan laboratory.
And US Secretary of State Mike Pompeo on Sunday said "enormous evidence" backed up that claim, which China has vehemently denied.
"Like any evidence-based organization, we would be very willing to receive any information that purports to the origin of the virus," Ryan said, stressing that this was "a very important piece of public health information for future control.
"If that data and evidence is available, then it will be for the United States government to decide whether and when it can be shared, but it is difficult for the WHO to operate in an information vacuum in that regard," he added.
The UN agency also hails the fundraising efforts of a teleconference of world leaders to boost development of a coronavirus vaccine, but warns that the money raised would only cover part of the ongoing response against the pandemic saying "this virus will be with us for a long time".
(Source: Reuters)
***
Risto Koivula
02.06.2021 15:08:40
405442
WHO kiisti jo helmikuussa "Wuhanin-("bioase)laboratiorioteoria - EIKÄ SE SIIHEN OLE MYÖHEMMINKÄÄN SIIRTYNYT!
https://www.presstv.com/Detail/2021/02/09/644910/WHO-refutes-Wuhan-lab-claim-about-coronavirus-origin
WHO refutes Wuhan lab claim about coronavirus origin
Tuesday, 09 February 2021 5:22 PM

World Health Organization (WHO) expert researcher Peter Ben Embarek speaks during a press conference to wrap up a visit by an international team of experts, in the city of Wuhan, in China's Hubei Province, on February 9, 2021. (Photo by AFP)
A team of experts from the World Health Organization (WHO) investigating the origins of the COVID-19 pandemic have dismissed a controversial theory that the virus leaked from a laboratory in the Chinese city of Wuhan.
The WHO fact-finding mission, which has been in China over the past two weeks to probe the origins of the pandemic, announced during a media briefing on Tuesday that the possibility of the virus having leaked from a lab was “extremely unlikely” and did not require further study.
Peter Ben Embarek, the head of the WHO team, said Beijing had granted “full access” to all sites and personnel they had requested to conduct a comprehensive investigation.
The WHO fact-finding mission arrived in Wuhan last month and visited key sites, including the Huanan seafood market, the location of the first known cluster of infections, as well as the Wuhan Institute of Virology, which was said by some to have been the actual origin of the virus.
The institute and the Chinese government had already rejected the allegation.
Since the outbreak of the epidemic, the origin of the new coronavirus has been widely discussed online, and conspiracy theories have emerged around it.
The pandemic became a political tool at the hands of former US president Donald Trump, who routinely called the pathogen “the Wuhan virus.”
WHO, intel reject Trump, Pompeo’s claim COVID-19 came from Wuhan lab
The World Health Organization says the US had provided no evidence to support US President Donald Trump’s claim that the coronavirus originated in a Chinese lab.

Trump and his associates also claimed that there had been evidence that Beijing created the new coronavirus in the medical lab in the Chinese city, even though the US intelligence agencies said they had seen no such evidence.
The coronavirus pandemic has so far claimed the lives of nearly 2,341,000 people and infected well over 107,147,260 across the world.
Wuhan lab director says virus leak claims ‘pure fabrication’
The Wuhan Institute of Virology has dismissed US claims that the coronavirus may have leaked from there.
The WHO team also said there had been no indication of the transmission of the new coronavirus in Wuhan before December 2019, when the first official cases of COVID-19 were recorded.
“In trying to understand the picture of December 2019, we embarked on a very detailed and profound search for other cases that may have been missed, cases earlier on in 2019,” said Embarek.
“And the conclusion was we did not find evidence of large outbreaks that could be related to cases of COVID-19 prior to December 2019 in Wuhan or elsewhere,” he added.
Embarek also said the team had not identified an animal source and that the virus could have been circulating in other regions before it was identified in Wuhan.
Speaking alongside Embarek, head of China’s expert panel on the outbreak, Liang Wannian, also said that early data suggested that the coronavirus could have been circulating for “several weeks” before it was identified in Wuhan.
“This indicates the possibility of the missed reported circulation in other regions,” Liang said, adding that there was “no evidence” to suggest the virus had been spreading in Wuhan before December 2019.
Press TV’s website can also be accessed at the following alternate addresses:
http://www.presstv.ir
http://www.presstv.co.uk
http://www.presstv.tv "
***
Risto Koivula
03.06.2021 00:28:22
405448
WHO: Koronaa oli Italiassa ennen kuin siitä raportoitiin Kiinassa:
https://sputniknews.com/europe/202106021083060943-who-revisits-puzzling-covid-positive-blood-samples-from-pre-pandemic-italy-in-origins-hunt/
" Europe
WHO Revisits Puzzling COVID-Positive Blood Samples From Pre-Pandemic Italy in Origins Hunt
19:51 GMT 02.06. 2021
by Morgan Artyukhina

The World Health Organization’s initial investigation into the origins of the COVID-19 pandemic found little reason to believe the virus leaked from a Chinese biolab, but didn’t outright dismiss the idea, either. Nonetheless, anti-China figures have continued to push the theory as being equal in validity to others, like zoonotic transfer.
WHO scientists are taking a harder look at a set of blood tests taken in Italy in October 2019 that later tested positive for antibodies against SARS-CoV-2, the virus that causes COVID-19.
On Tuesday, WHO officials confirmed they were in contact with a group of scientists in Italy who published a shocking report last November revealing that several blood tests collected as part of a lung cancer screening program months before the first cases of COVID-19 were detected in Italy had mysteriously tested positive for antibodies the body produces to fight SARS-CoV-2.
Their report, published by the Italian National Cancer Institute in its magazine Tumori Journal, found that 111 of 959 samples in the trial showed the unique spike protein SARS-CoV-2 uses to infect cells in the human body were present in the patient’s blood, and that tests of other similar coronaviruses were negative. That would mean that the patients had contracted and recovered from COVID-19 by the time of the October blood tests, signaling that COVID-19 was circulating in northern Italy in September 2019 - six months before the first cases were detected in Milan in February 2020.
"The WHO asked us if we could share the biological material and if we could re-run the tests in an independent laboratory. We accepted," Giovanni Apolone, scientific director of the Milan Cancer Institute (INT), one of the institutions responsible for the November 2020 paper, told Reuters on Monday.
According to Reuters, both positive and negative samples have been sent to Erasmus University in Rotterdam, the Netherlands, to be re-tested.
Apolone stressed that "none of the studies published so far have ever questioned the geographical origin," but likely indicate a less lethal variant of the virus has been in circulation for some time since the slew of deadlier, more virulent cases attracted medical attention in the Chinese city of Wuhan in the final days of 2019.
By February 21, 2020, the first case of COVID-19 in Europe was detected in Milan, Italy, and the city became the epicenter of Italy’s outbreak. Italy suffered the worst of the first wave of the pandemic in Europe, with a death rate as high as 7.2% - twice the death rate reported in Hubei Province, where the outbreak was first recor-ded. However, there are indications the pandemic in Italy was even worse in 2020 than reported, according to an Italian study published in January.
However, even if a milder COVID-19 infection was circulating in China earlier in 2019, it would still seem to disprove the once-discredited theory, now revived by the Biden administration, that SARS-CoV-2 escaped from the Wuhan Institute of Virology. As Sputnik has reported, the theory was spread by former US President Donald Trump and right-wing anti-China figures close to him in early 2020 as the pandemic spiraled out of control in the US and his administration began looking for someone else to blame for it.
Last week, WHO spokesperson Fadela Chaib told a United Nations briefing the agency was preparing a proposal on a second phase of its investigation into the origins of SARS-CoV-2, but she provided no specific timeline. The first phase, con-ducted in January and February and released in March,yielded no concrete results, but found a zoonotic exchange - that humans caught it from an infected animal - more likely than that the virus escaped from the Wuhan lab. They also suggested an international military sports tournament the city hosted in October 2019 be investigated as an additional possible vector.
Some scientists and political figures intent on pushing the “lab leak” theory have claimed Beijing denied the WHO scientists adequate access to data from the Wu-han virology lab, with more than a dozen US allies issuing a statement demanding openness, but scientists on the WHO team have pushed back, saying their efforts weren’t impeded by Chinese officials, and that the level of openness being deman-ded of China is one no Western country would accept if it were made of them.
Also last week,US President Joe Biden ordered an intelligence report on the origins of COVID-19, "including whether it emerged from human contact with an infected animal or from a laboratory accident,” to be delivered in 90 days. In response, the Global Times called for the US biolab at Fort Detrick, Maryland, to be investigated as well. "
Risto Koivula
03.06.2021 23:45:58
405453
WHO: Koronaa oli Italiassa ennen kuin siitä raportoitiin Kiinassa:
Lainaus: riiviö, 03.06.2021 17:41:37, 405450
Sen vaan totean, että pitkät suorat lainaukset ilman mitään omaa kontribuutiota ovat aivan perseestä tällä foorumilla.
Linkki riittää mainiosti ja sitten se oma asia, jos sitä on ja jos sen osaa kirjottaa.
Tulipa sanotuksi. Helpotti. En ole täällä ollenkaan moderointitehtävissä.
RK: Linkit menee kiinni ja tunnusten taakse. Tätä asiaa on syytä voida seurata 10:nkin vuoden päästä.
Risto Koivula
04.06.2021 02:36:34
405456
HEWOWWITTUA, YLE!!! SITÄ *EI* OLE "MUOKATTU"!!!
Sähköpostit paljastavat: Tutkija varoitti varhain Yhdysvaltain korona-asiantuntija Anthony Faucia, että virusta on mahdollisesti muokattu
Buzzfeedin julkaisemien sähköpostien perusteella Faucilla oli syytä pitää laboratoriovuotoa uskottavana vaihtoehtona koronaviruksen alkuperälle.

Anthony Fauci
Kansallisen allergia- ja infektiotautien instituutin pääjohtaja Anthony Fauci toimii Valkoisen talon korona-asiantuntijana.Stefani Reynolds / EPA
3.6. 16:46
Yhdysvaltalaisen tartuntatautien tutkimuslaitoksen johtaja lähetti Valkoisen talon ko-rona-asiantuntija Anthony Faucille tammikuun 2020 lopussa sähköpostin, jossa hän kertoi, että pieni osa koronaviruksen perimästä näyttää mahdollisesti muokatulta.
Asia selviää Faucin sähköposteista, jotka Buzzfeed-sivusto sai haltuunsa tietopyyn-nön kautta. Myös Washington Post (siirryt toiseen palveluun) on hankkinut Faucin sähköposteja itselleen.
Buzzfeed on ladannut yli 3 200 sivua sähköposteja nettiin kaikkien tarkasteltaviksi. (siirryt toiseen palveluun) Viestit ovat tammi-kesäkuulta 2020.
Fauci tyrmäsi julkisesti keväällä 2020 teorian siitä, että pandemian aiheuttanut Sars-Cov-2 -koronavirus olisi peräisin kiinalaisesta laboratoriosta.
Buzzfeedin saamien sähköpostien perusteella hänellä kuitenkin näytti olleen syytä pitää laboratoriovuotoa uskottavana vaihtoehtona viruksen alkuperälle.
Tutkijat kiinnittivät huomiota viruksen erityispiirteisiin
Immunologian ja mikrobiologian professori Kristian G. Andersen kirjoitti Faucille 31. tammikuuta 2020 lähettämässään sähköpostissa, että hän ja kolme kollegaa katsovat viruksen geeniperimän vaikuttavan epäjohdonmukaiselta evoluutioteoriaan liittyvien odotusten kannalta.
Hän toimii Scrippsin tutkimusinstituutin Andersen Labin johtajana.
– Viruksen epätavalliset erityispiirteet muodostavat todella pienen osan geeniperi-mästä (<0,1%), joten kaikkia sekvenssejä täytyy tarkastella hyvin tarkasti, jotta voi nähdä, että osa ominaisuuksista (mahdollisesti) näyttää muokatuilta, Andersen kirjoitti.
Andersen kertoi, että evoluutiopuussa virus näyttää täysin normaalilta ja se näyttäisi olevan peräisin lepakoista.
Andersen lisäsi, että asia vaati lisää analyyseja ja heidän mielipiteensä voivat vielä muuttua.
Lyhyessä vastausviestissään Fauci kiittää Andersenia ja sanoo, että keskustellaan pian puhelimitse. Hän ei tuonut tutkijoiden näkemystä julki.
Andersen pitää nyt laboratoriovuotoa epätodennäköisenä
Myöhemmin professori Kristian G. Andersenin mielipide muuttui.
Hänen ryhmänsä julkaisi maaliskuussa 2020 Nature-lehdessä (siirryt toiseen palve-luun) tutkimuksen, jonka mukaan on epätodennäköistä, että Sars-Cov-2 on syntynyt Sarsin kaltaisen koronaviruksen muokkauksen tuloksena.
Huhtikuussa 2021 Andersen avasi Twitterissä näkemystään, miksi hän pitää labora-toriovuotoa epätodennäköisenä. Andersen kertoi, että he etsivät merkkejä viruksen muokkauksesta laboratoriossa, mutta eivät löytäneet siihen viittaavia todisteita.
Andersen sanoi, että jos laboratoriovuototeoria pitäisi paikkansa, se vaatisi suurta peittelyä ja valehtelua monilta arvostetuilta tutkijoilta Kiinassa ja muualla.
– Todistaako raportti varmasti, että laboratoriovuotoa ei tapahtunut? Ei todista. Tarkoittaako se, että meidän ei tulisi harkita laboratoriovuodon mahdollisuutta? Ei tarkoita. Sen sijaan rapotin johtopäätös on, että se on erittäin epätodennäköinen, koska muut hypoteesit ovat paljon todennäköisempiä, Andersen kirjoitti Twitterissä.
Lisäksi Andersen sanoi, että pandemian alkuperä vaatii lisää avoimia tutkimuksia. Hän arvioi, että ne todennäköisesti kestävät vuosia.
"Salaliittoteoria" kiinnosti Faucin pomoa
Yhdysvaltain terveysviraston NIH:n johtaja Francis Collins lähetti 16. huhtikuuta 2020 Faucille ja muutamalle muulle terveysviranomaiselle sähköpostin otsikolla "salaliitto kerää vauhtia".
Fauci toimii terveysviraston alaisen kansallisen allergia- ja infektiotautien instituutin pääjohtajana. Collins on Faucin pomo.
Collinsin viestissä oli linkki Mediaite-sivuston uutiseen, joka käsitteli Fox News-kanavalla käytyä keskustelua viruksen mahdollisesta karkaamisesta wuhanilaisesta laboratoriosta.
Collinsin viestin sisältö on mustattu Buzzfeedin saamista sähköposteista yllä mainittua linkkiä lukuunottamatta. Fauci vastasi Collinsille, mutta myös hänen vastauksensa on peitetty.
Wuhanilaislaboratorion kumppanilta kiitokset
Pari päivää myöhemmin, 18. huhtikuuta 2020, Fauci sai sähköpostin brittiläiseltä eläintieteilijältä Peter Daszakilta, joka johtaa EcoHealth Alliance -tutkimusjärjestöä.
Daszak kirjoitti haluavansa kiittää Faucia henkilökuntansa ja yhteistyötahojensa puo-lesta siitä, että Fauci oli julkisesti sanonut tieteellisen todistusaineiston tukevan sitä, että Covid-19 on tarttunut luonnollisella tavalla lepakoista ihmisiin eikä ole karannut Wuhanin virologisen instituutin laboratoriosta.

Suuri osa viestistä on peitetty. Lopuksi Daszak kehuu, että Faucin rohkeat kommentit auttavat kumoamaan väitteitä viruksen alkuperästä.
Fauci vastasi, että paljon kiitoksia ystävällisestä viestistäsi.
Daszakin johtama EcoHealth Alliance on tehnyt vuosia läheistä yhteistyötä Wuhanin virologisen instituutin kanssa koronavirusten tutkimuksessa.
Monet ihmiset kyselevät nyt Twitterissä Daszakilta, mitä viestin peitetyssä osassa sanottiin. Toiset syyttävät häntä murhaajaksi, koska he katsovat hänen olevan osasyyllinen pandemiaan.
Laboratorioalkuperä noussut vaihtoehdoksi viime aikoina (Valetta, pelkkää hörölöröä)
Fauci sanoi viime kuussa lainsäätäjille,että Yhdysvaltain terveysvirasto oli myöntänyt 600 000 dollarin apurahan Wuhanin virologiselle instituutille. Rahoitus oli ohjattu kiinalaislaboratoriolle juuri EcoHealth Alliancen kautta.
Viisivuotisen apurahan avulla oli tarkoitus tutkia koronavirusten tarttumista lepakois-ta ihmisiin, jotta tutkijat ymmärtäisivät paremmin 2000-luvun alkupuolen Sars-epidemiaa. Trumpin hallinto keskeytti rahoituksen viime vuonna.
Peter Daszak kertoi joulukuussa 2019 podcast-haastattelussa (siirryt toiseen palveluun), että koronaviruksia voi muokata melko helposti laboratoriossa.
Daszak kuului Maailman terveysjärjestö WHO:n tutkimusryhmään, joka yritti selvittää koronapandemian lähdettä Wuhanissa. Hän on myös jäsen tieteellisen Lancet-julkaisun ryhmässä, joka selvittää pandemian alkuperää.
Daszakia on arvosteltu eturistiriidasta kaksoisroolinsa vuoksi. Hän on kutsunut viruksen mahdollista karkaamista wuhanilaislaboratoriosta salaliittoteoriaksi.
Viruksen mahdollinen laboratorioalkuperä on noussut varteen otettavaksi vaihtoehdoksi viime aikoina.
Wall Street Journal -lehti (siirryt toiseen palveluun) uutisoi toukokuussa, että kolme Wuhanin virologisen instituutin työntekijää joutui marraskuussa 2019 sairaalaan, koska heillä oli koronatartuntaan viittaavia oireita.
Fauci kannattaa lisätutkimuksia
Anthony Fauci sanoi toukokuussa senaatille, että hän ja suurin osa tieteellisestä yhteisöstä pitää todennäköisimpänä skenaariona, että Sars-Cov-2 on peräisin luonnosta, mutta kukaan ei voi olla siitä täysin varma.
CNN:n mukaan (siirryt toiseen palveluun) Fauci sanoi haastattelussa, että hän ei ole vakuuttunut siitä, että virus olisi syntynyt luonnollisesti. Fauci sanoi kannattavansa tutkimusta siitä, mitä Kiinassa tapahtui.
Presidentti Joe Biden on määrännyt Yhdysvaltain tiedustelupalvelut selvittämään, pääsikö virus karkuun kiinalaisesta laboratoriosta.
Asian selvittämistä hankaloittaa se, että Kiina ei ole suostunut avoimeen kansainväli-seen tutkintaan. Kiina on kiistänyt viruksen karkaamisen laboratoriosta ja on kutsunut väitettä salaliittoteoriaksi.
Lue lisää:
Yhdysvallat rahoitti virustutkimusta wuhanilaisessa laboratoriossa – osa republikaaneista vaatii nyt korona-asiantuntija Anthony Faucin eroa
Jani Kaaron kolumni: Entäpä jos koronavirus onkin laboratoriokarkulainen Wuhanin viruslaboratoriosta? (täyttä paskaa)
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https://www.forbes.com/sites/davidnikel/2020/06/07/controversial-coronavirus-lab-origin-claims-dismissed-by-experts/
ForbesLifestyle Travel Editors' Pick
Jun 7, 2020,03:42pm EDT

Wuhan Institute of Virology is one of China's leading research centres and has been the subject of ... [+]
AFP via Getty Images
June 8: This article has been substantially updated to reflect criticism of the published study, along with the general scientific consensus on Covid-19. It also clarifies Sørensen’s financial interest in the development of the Biovacc-19 coronavirus vaccine. This context did not appear in the original post. June 10: Updated with additional comment from Gunnveig Grødeland.
New claims that the novel coronavirus SARS-CoV-2 was engineered have been dismissed by scientific and intelligence experts.
The authors of a British-Norwegian vaccine study—accepted by the Quarterly Review of Biophysics — claim that the coronavirus's spike protein contains sequences that appear to be artificially inserted.
In their paper, the Norwegian scientist Birger Sørensen and British oncologist Angus Dalgleish claim to have identified "inserted sections placed on the SARS-CoV-2 spike surface" that explains how the virus interacts with cells in the human body. Virologists, however, note that similar sections appear naturally in other viruses.
Accidental release claims challenged
Sir Richard Dearlove, who was head of MI6 from 1999 to 2004, told the Daily Telegraph that Sørensen and Dalgleish’s research shows that the pandemic may have started at the Wuhan Institute of Virology. He added that he thought it unlikely to have been released deliberately, but that China had clearly tried to cover up the release.
However, intelligence sources from Britain’s MI5 dismissed the idea as “rumor and conspiracy,” according to the Times of London. Dearlove was previously criticized in the Chilcot Inquiry into the Iraq War for promoting “flawed intelligence.”
Since the coronavirus took hold in the United States, senior officials in the Trump administration have amplified rumors that the virus emerged from a virology lab in Wuhan. However, public health researchers have traced the earliest recorded cases of the virus to an animal market in the city.
Management at the Wuhan Institute of Virology have previously told Chinese state television that such claims were “total fabrication” and that the lab had not encountered SARS-CoV-2 until samples from patients with an then unidentified pneumonia-like disease were referred to them in December.
Scientific claims questioned
Sørensen and Dalgleish’s work contradicts the international scientific consensus that although the coronavirus pandemic originated in Wuhan, there is no evidence that it had been artificially engineered.
An analysis of the first 41 Covid-19 patients published in medical journal the Lancet found that in 27 cases, there had been direct exposure to the Wuhan market, although not with the first known case. The World Health Organization has since released guidance to those working in and visiting such markets, to reduce animal-human transmission of emerging pathogens.
The report’s authors also claim the lack of mutation in the virus since its discovery, suggests it was already fully adapted to humans. However, there have been several published studies noting evolution and mutation among SARS-CoV-2 strains.
Sørensen told Norwegian broadcaster NRK that the virus has properties that differ greatly from SARS, another coronavirus, and have never been detected in nature. He claimed that China and the United States have collaborated for many years on coronavirus research through "gain of function" studies, in which the pathogenicity or transmissibility of potential pandemic pathogens can be enhanced in order to understand them better.
Examples found in other viruses
Gunnveig Grødeland, vaccine researcher at the University of Oslo, is one of the scientists voicing their disagreement with Sørensen. She explains that what Sørensen referred to as "inserted sequences" can enable the development of a more serious disease, but this is not unusual in nature: "Examples can be found in other viruses including subtypes of influenza (including "bird flu"), HIV, and several human coronaviruses (MERS, OC43, HKU1)." Grødeland also says that Sørensen's paper offered no biological confirmation on the relevance of positively charged patches.
Other leading voices in the scientific community and fight against the pandemic have dismissed claims that the coronavirus was man-made. Anthony Fauci, director of U.S. National Institute of Allergy and Infectious Diseases, has stated there is no scientific evidence for the claims, while leading researchers from the World Health Organization and Galveston National Laboratory also dismissed the rumours.
The report was allegedly previously rejected
The Telegraph claimed that the study was initially rejected by several academic journals, including "Nature" and "Journal of Virology," which indicates they considered the article unsuitable for publication. Sørensen claimed the original study tied the vaccine development to the origin research, and that they have since split the research. He claimed a second study with more details on the origin of the virus will be published soon.
The report published in the Quarterly Review of Biophysics explains the rationale for the development of Biovacc-19, a candidate vaccine for COVID-19 that is now in advanced preclinical development. Sørensen has a financial interest in Immunor, the Norwegian company behind the vaccine.
No, COVID-19 Coronavirus Was Not Bioengineered. Here’s The Research That Debunks That Idea (Forbes)
Fauci, Top U.S. General Throw Cold Water On Trump’s Coronavirus Claim (Forbes)
The Controversial Rumor COVID-19 Originated In A Wuhan Lab Creeps Into The GOP Mainstream (Forbes)
A Timeline Of The COVID-19 Wuhan Lab Origin Theory (Forbes)
Follow me on Twitter. Check out my website or some of my other work here.
I was born in the U.K. but moved to Norway in 2011 and haven't looked back. I run a website and podcast about Norway, authored the Moon Norway travel guidebook, and spend my free time touring the country to discover more about the people and places of this unique corner of the world. I write for Forbes with an outsider's inside perspective on Norway & Scandinavia.
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Haistapaskantiede-Birger Sørensenin "todistus":
https://www.nrk.no/norge/norsk-forsker-skaper-strid-om-virusets-opphav_-_-dette-viruset-har-ikke-en-naturlig-opprinnelse-1.15043634
NRK skrev at studien som omtales i denne saken var publisert i det anerkjente tidsskriftet Quarterly Review of Biophysics. Det riktige er at studien ble publisert i QRB Discovery, som er en nyetablert søster-publikasjon.
Det fremgikk ikke av den opprinnelige saken at studien skal publiseres i to forskningsartikler, hvorav kun den ene så langt er publisert. Ifølge forsker Birger Sørensen omhandler den første forskningsartikkelen vaksineutvikling, mens den andre omhandler virusets opphav.
Artikkelen er oppdatert med en kommentar fra John Fredrik Moxnes, og med forbehold om forskernes funn.
I en fersk studie publisert i tidsskriftet QRB Discovery skriver den britiske professoren Angus Dalgleish og den norske forskeren Birger Sørensen om det såkalte spike-proteinet i koronaviruset. Ifølge forskerne kan sekvenser i dette proteinet tyde på at viruset ikke har et naturlig opphav.
INSERTS: Dette er sekvensene Sørensen mener peker mot at viruset ikke har naturlig opphav. Sekvensene ble først beskrevet av kinesiske forskere.
Foto: Faksimile / QRB Discovery Quarterly
Forskerduoen påpeker også at viruset nesten ikke har mutert siden det begynte å smitte mellom mennesker, noe som tyder på at det allerede var ferdig tilpasset mennesker. Dette er ifølge Sørensen helt uvanlig for virus som krysser artsbarrierer.
Ifølge Sørensen har viruset egenskaper som skiller seg kraftig fra SARS, og som aldri tidligere er påvist i naturen.
– Når vi teknisk beskriver viruset så ser vi jo at det ikke har blitt til ved en naturlig utvikling. Det er gjort av amerikanere og kinesere, som del av det som heter «gain of function»-studier. Det gjøres over hele verden. Man sier man ikke gjør det, men det skjer hele tiden på avanserte laboratorier, ifølge Sørensen.
Kina og USA har i mange år samarbeidet om forskning på koronavirus. I såkalte gain of function-forsøk øker man virusets smittsomhet på en kunstig måte, for å gjøre viruset enklere å bruke i vitenskapelige eksperimenter. Slike manipulerte virus kalles «chimera».
Britisk spionsjef: – Et labuhell
De siste dagene har Sørensens funn skapt heftig debatt i britisk presse.
Sir Richard Dearlove, som var sjef for den britiske utenlandsetterretningen MI6 fra 1999 til 2004, sier til avisen Daily Telegraph at arbeidet til forskerduoen viser at pandemien som lammer verden kan ha startet i et laboratorium.
ET LABUHELL: Britenes tidligere spionsjef Sir Richard Dearlove tror koronaviruset slapp ut fra en lab, og viser til arbeidet Birger Sørensen har gjort.
Foto: Håvard Blekastad Almås / NRK
– Jeg tror dette startet som et uhell. Dermed reises spørsmålet om Kina kommer til å påta seg ansvar, og om Kina skal betale erstatning. Jeg tror dette vil få alle land til å tenke gjennom sitt forhold til Kina og hvordan de forholder seg til Kinas lederskap, sier Dearlove til avisen.
En talsmann for Downing Street svarer imidlertid på Dearloves utspill med at det idag ikke finnes noen bevis for at koronaviruset er menneskeskapt.
I flere måneder har det versert påstander om at viruset kan ha lekket ut fra laboratoriet til det virulogiske instituttet i Wuhan, ett av Kinas mest avanserte viruslaboratorier.
Påstandene tilbakevises fullstendig av instituttledelsen, som hevder laboratoriet aldri har vært i besittelse av virus som i det hele tatt ligner på SARS-CoV-2.
– Dette er ren fabrikasjon. Vårt institutt mottok de første kliniske prøvene med dette viruset 30. desember, sier instituttsjef Wang Yanyi til den kinesiske statlige TV-stasjonen CGTN.
Wuhans virologiske institutt er ett av Kinas mest avanserte viruslaboratorier med den høyeste sikkerhetsklassifiseringen, såkalt P4.
Foto: HECTOR RETAMAL
Kina har fremdeles ikke identifisert indeks-pasienten, eller det nøyaktige stedet der utbruddet startet. Kinesisk CDC har gjort undersøkelser av de første smittede rundt fiskemarkedet i Wuhan som tyder på at smitten ikke oppstod der.
Sørensen mener imidlertid det er kinesiske forskere som først har omtalt de modifiserte sekvensene i virusoverflaten. Men de siste måndene mener han Kina har lagt lokk på alle slike studier.
– De innsatte sekvensene skulle aldri vært publisert. Hadde det vært idag, ville det aldri skjedd. Det var en stor feil kineserne gjorde. De innsatte sekvensene har en funksjonalitet som vi beskriver. Vi forklarer hvorfor de er vesentlige. Men kineserne pekte på dem først, sier Sørensen.
I studien takker Sørensen sjefsforsker John Fredrik Moxnes ved Forsvarets Forskningsinstitutt (FFI) for «uvurderlig hjelp» i arbeidet.
Moxnes sier han har brukt sin kunnskap om regnekraft til å samarbeide med Sørensen og hans firma Immunor i vaksineutvikling.
– Moderne vaksineutvikling dreier seg om regnekraft og bioteknologi som det er viktig at Norge er delaktig i, sier Moxnes til NRK.
Tror ikke vaksinekandidater vil virke
Sørensen tror de nåværende vaksinekandidatene vil ha stor risiko for bivirkninger, fordi de sikter mot virusets såkalte spike-protein, der 80% av arvestoffet er såkalte human-likt.
– 78.4% av epitopene i spike-proteinet er identisk med oss som mennesker. Og konsekvensen av det er at det er 78.4% sannsynlighet for å få bivirkning i en eller annen form av vaksiner som retter seg inn mot dette proteinet.
Vaksineforsøk mot virus som Dengue-feber og HIV har vist betydelig risiko for at vaksinene faktisk kan føre til mer alvorlig sykdom, gjennom en prosess som kalles antistoff-avhengig forsterkning (ADE).
Sørensen jobber nå med å utvikle en egen vaksinekandidat kalt Biovacc-19, som sikter seg inn mot de 20% av virus-arvestoffet som ikke deles av mennesker.
Det har imidlertid vært liten norsk interesse for å finansiere et vaksineforsøk her til lands.
– Vi deltar ikke i det store spillet rundt å være først til mål. Det vi har laget er en vaksinekandidat som er grunnleggende forskjellig fra alle andre. De beste vaksinene vil uansett bli finansiert og vinne frem, sier Sørensen.
Publisert 7. juni 2020 kl. 19:49 Oppdatert 8. juni 2020 kl. 18:34
https://usrtk.org/scientific-papers-on-the-origins-of-sars-cov-2/
" Scientific papers on the origins of SARS-CoV-2
Posted: February 23, 2023 by Hana Mensendiek
Here is a list of papers published in peer-reviewed scientific journals on the origins of SARS-CoV-2, the virus that causes COVID-19.
Science. The Huanan Seafood Wholesale Market in Wuhan was the early epicenter of the COVID-19 pandemic. By Michael Worobey et al. July 26, 2022.
Science. The molecular epidemiology of multiple zoonotic origins of SARS-CoV-2. By Jonathan E. Pekar et al. July 26, 2022.
Nature. Wuhan market was epicentre of pandemic’s start, studies suggest. By Amy Maxmen. February 27, 2022.
Zenodo. The Huanan market was the epicenter of SARS-CoV-2 emergence. Michael Worobey et al. February 26, 2022.
Zenodo. SARS-CoV-2 emergence very likely resulted from at least two zoonotic events. Jonathan Pekar et al. February 26, 2022.
Nature Portfolio. Surveillance of SARS-CoV-2 in the environment and animal samples of the Huanan Seafood Market. George Gao et al. February 25, 2022.
Nature Portfolio. Coronaviruses with a SARS-CoV-2-like receptor-binding domain allowing ACE2-mediated entry into human cells isolated from bats of Indochinese peninsula. Sarah Temmam et al. September 17, 2021. Under review.
Nature.Origins of SARS-CoV-2: window is closing for key scientific studies. August 25, 2021.
Cell. The Origins of SARS-CoV-2: A Critical Review (pre-proof). Edward C. Holmes et al. August 20, 2021.
Science. The animal origin of SARS-CoV-2. Spyros Lytras,Wei Xia,Joseph Hughes,Xiaowei Jiang andDavid L. Robertson. August 17, 2021.
mBio. Can Science Help Resolve the Controversy on the Origins of the SARS-CoV-2 Pandemic? Arturo Arturo Casadevall, Susan R. Weiss and Michael Imperiale. August 2, 2021.
Independent Science News. Phylogeographic Mapping of Newly Discovered Coronaviruses Pinpoints the Direct Progenitor of SARS-CoV-2 as Originating from Mojiang, China. Jonathan Latham and Allison Wilson. August 2, 2021.
Frontiers in Public Health. Lethal Pneumonia Cases in Mojiang Miners (2012) and the Mineshaft Could Provide Important Clues to the Origin of SARS-CoV-2. Alex C. Speciale. July 13, 2021.
Medium. A response to “The Origins of SARS-CoV-2: A Critical Review.” Alina Chan. July 12, 2021.
Nature Scientific Reports. In silico comparison of SARS-CoV-2 spike protein-ACE2 binding affinities across species and implications for virus origin. Sakshi Piplani, Puneet Kumar Singh, David A. Winkler, Nikolai Petrovsky. June 24, 2021. doi: https://doi.org/10.1038/s41598-021-92388-5
bioRxiv. Recovery of deleted deep sequencing data sheds more light on the early Wuhan SARS-CoV-2 epidemic. Jesse Bloom. June 22, 2021. doi: https://doi.org/10.1101/2021.06.18.449051
In Vivo. On the Origin of SARS-CoV-2: Did Cell Culture Experiments Lead to Increased Virulence of the Progenitor Virus for Humans? Bernd Kaina. May 2021, 35 (3) 1313-1326; DOI: https://doi.org/10.21873/invivo.12384
Infectious Diseases & Immunity. Origins of SARS-CoV-2: Focusing on Science. Zhengli Shi. April 2021 – Volume 1, Issue 1, p.3-4 doi: 10.1097/ID9.0000000000000008
Environmental Chemistry Letters. Should we discount the laboratory origin of COVID-19? Rossana Segreto, Yuri Deigin, Kevin McCairn, Alejandro Sousa, Dan Sirotkin, Karl Sirotkin, Jonathan J. Couey, Adrian Jones & Daoyu Zhang. March 25, 2021.
Environmental Chemistry Letters. Tracing the origins of SARS-COV-2 in coronavirus phylogenies: a review. Erwan Sallard, José Halloy, Didier Casane, Etienne Decroly and Jacques van Helden. February 4, 2021. doi: https://doi.org/10.1007/s10311-020-01151-1
Zenodo. A Bayesian analysis concludes beyond a reasonable doubt that SARS-CoV-2 is not a natural zoonosis but instead is laboratory derived. Dr. Steven Quay. January 29, 2021.
Nature. Addendum: A pneumonia outbreak associated with a new coronavirus of probable bat origin. Peng Zhou, Xing-Lou Yang, Xian-Guang Wang, Ben Hu,…and Zheng-Li Shi. November 17, 2020. https://doi.org/10.1038/s41586-020-2951-z
BioEssays. The genetic structure of SARS‐CoV‐2 does not rule out a laboratory origin. Rossana Segreto and Yuri Deigin. November 17, 2020. https://doi.org/10.1002/bies.202000240
Zenodo. Where Did the 2019 Coronavirus Pandemic Begin and How Did it Spread? The People’s Liberation Army Hospital in Wuhan China and Line 2 of the Wuhan Metro System Are Compelling Answers. Steven Carl Quay. October 28, 2020. doi: 10.5281/zenodo.4119262
Frontiers in Public Health. Lethal pneumonia cases in Mojiang miners (2012) and the mineshaft could provide important clues to the origin of SARS-CoV-2. Monali Rahalkar and Rahul Bahulikar. September 17, 2020. doi: 10.3389/fpubh.2020.581569
Journal of Medical Virology. Questions concerning the proximal origin of SARS-CoV-2. Murat Seyran, Damiano Pizzol, Parise Adadi…and Adam M. Brufsky. September 3, 2020. doi: https://doi.org/10.1002/jmv.26478
BioEssays. Might SARS‐CoV‐2 have arisen via serial passage through an animal host or cell culture? Karl Sirotkin and Dan Sirotkin. August 12, 2020. https://doi.org/10.1002/bies.202000091
bioRxiv. SARS-CoV-2 is well adapted for humans. What does this mean for re-emergence? Shing Hei Zhan, Benjamin E. Deverman, Yujia Alina Chan. May 2, 2020. doi: https://doi.org/10.1101/2020.05.01.073262
Nature Medicine. The proximal origin of SARS-CoV-2. Kristian G. Andersen, Andrew Rambaut, W. Ian Lipkin, Edward C. Holmes, Robert F. Garry. April 2020. Volume 26, pages 450-455.
Antiviral Research. The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade. Bruno Coutard et al. February 10, 2020. DOI: 10.1016/j.antiviral.2020.104742
Nature. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Peng Zhou, Xing-Lou Yang, Xian-Guang Wang, Ben Hu,…and Zheng-Li Shi. February 3, 2020. 579(7798): 270-273. doi:10.1038/s41586-020-2012-7
Preprint. The possible origins of 2019-nCoV coronavirus. Botao Xiao. February 2020. doi: 10.13140/RG.2.2.21799.29601
The Lancet. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Chaolin Huang et al. January 30, 2020. Volume 395: 497–506.
Scientific Reports. Animal sales from Wuhan wet markets immediately prior to the COVID-19 pandemic. Xiao Xiao et al. June 7, 2021. Sci Rep 11, 11898 (2021). https://doi.org/10.1038/s41598-021-91470-2
Minerva. The evidence which suggests that this is no naturally evolved virus: A reconstructed historical aetiology of the SARS-CoV-2 spike. Birger Sørensen, Angus Dalgleish & Andres Susrud. July 1, 2020.
ResearchGate. Is considering a genetic-manipulation origin for SARS-CoV-2 a conspiracy theory that must be censored? Rossana Segreto and Yuri Deigin. April 2020. DOI: 10.13140/RG.2.2.31358.13129/1
Preprints. Major concerns on the identification of bat coronavirus strain RaTG13 and quality of related Nature paper. Xiaoxu Lin, Shizhong Chen. June 5, 2020. 2020060044. doi: 10.20944/preprints202006.0044.v1
Preprints. The abnormal nature of the fecal swab sample used for NGS analysis of RaTG13 genome sequence imposes a question on the correctness of the RaTG13 sequence. Monali Rahalkar and Rahul Bahulikar. August 11, 2020. doi: 10.20944/preprints202008.0205.v1
OSF Preprints. COVID-19, SARS and bats coronaviruses genomes unexpected exogeneous RNA sequences. Jean-Claude Perez and Luc Montagnier. April 25, 2020. doi:10.31219/osf.io/d9e5g
Zenodo. HIV man-manipulated coronavirus genome evolution trends. Jean-Claude Perez and Luc Montagnier. August 2, 2020.
Emerging Microbes & Infections. HIV-1 did not contribute to the 2019-nCoV genome. Xiao Chuan, Li Xiaojun, Liu Shuying, Sang Yongming, Gao Shou-Jiang and Gao Feng. 2020. 9(1): 378-381. doi: 10.1080/22221751.2020.1727299
Nature. Identifying SARS-CoV-2-related coronaviruses in Malayan pangolins. Tommy Tsan-Yuk Lam, Na Jia, Ya-Wei Zhang, Marcus Ho-Hin Shum, Jia-Fu Jiang, Hua-Chen Zhu, Yi-Gang Tong, Yong-Xia Shi, Xue-Bing Ni, Yun-Shi Liao, Wen-Juan Li, Bao-Gui Jiang, Wei Wei, Ting-Ting Yuan, Kui Zheng, Xiao-Ming Cui, Jie Li, Guang-Qian Pei, Xin Qiang, William Yiu-Man Cheung, Lian-Feng Li, Fang-Fang Sun, Si Qin, Ji-Cheng Huang, Gabriel M. Leung, Edward C. Holmes, Yan-Ling Hu, Yi Guan & Wu-Chun Cao. March 26, 2020. doi: https://doi.org/10.1038/s41586-020-2169-0
PLoS Pathogens. Are pangolins the intermediate host of the 2019 novel coronavirus (SARS-CoV-2)? Ping Liu, Jing-Zhe Jiang, Xiu-Feng Wan, Yan Hua, Linmiao Li, Jiabin Zhou, Xiaohu Wang, Fanghui Hou, Jing Chen, Jiejian Zou, Jinping Chen. May 14, 2020. doi: https://doi.org/10.1371/journal.ppat.1008421
Nature. Isolation of SARS-CoV-2-related coronavirus from Malayan pangolins. Kangpeng Xiao, Junqiong Zhai, Yaoyu Feng, Niu Zhou, Xu Zhang, Jie-Jian Zou, Na Li, Yaqiong Guo, Xiaobing Li, Xuejuan Shen, Zhipeng Zhang, Fanfan Shu, Wanyi Huang, Yu Li, Ziding Zhang, Rui-Ai Chen, Ya-Jiang Wu, Shi-Ming Peng, Mian Huang, Wei-Jun Xie, Qin-Hui Cai, Fang-Hui Hou, Wu Chen, Lihua Xiao & Yongyi She. May 7, 2020. doi: https://doi.org/10.1038/s41586-020-2313-x
Current Biology. Probable Pangolin Origin of SARS-CoV-2 Associated with the COVID-19 Outbreak. Tao Zhang, Qunfu Wu, Zhigang Zhang. March 19, 2020. doi: https://doi.org/10.1016/j.cub.2020.03.022
bioRxiv. Single source of pangolin CoVs with a near identical Spike RBD to SARS-CoV-2. Yujia Alina Chan and Shing Hei Zhan. October 23, 2020. doi: https://doi.org/10.1101/2020.07.07.184374
Infection, Genetics and Evolution. COVID-19: Time to exonerate the pangolin from the transmission of SARS-CoV-2 to humans. Roger Frutos, Jordi Serra-Cobo, Tianmu Chen and Christian A. Devaux. Volume 84, October 2020, 104493. https://doi.org/10.1016/j.meegid.2020.104493
bioRxiv. No evidence of coronaviruses or other potentially zoonotic viruses in Sunda pangolins (Manis javanica) entering the wildlife trade via Malaysia. Jimmy Lee, Tom Hughes, Mei-Ho Lee, Hume Field, Jeffrine Japning Rovie-Ryan, Frankie Thomas Sitam, Symphorosa Sipangkui, Senthilvel K.S.S. Nathan, Diana Ramirez, Subbiah Vijay Kumar, Helen Lasimbang, Jonathan H. Epstein, Peter Daszak. June 19, 2020. doi: https://doi.org/10.1101/2020.06.19.158717
Cell. A genomic perspective on the origin and emergence of SARS-CoV-2. Yong-Zhen Zhang, Edward C. Holmes. April 2020 181(2):223-227. doi: 10.1016/j.cell.2020.03.035.
Current Biology. A novel bat coronavirus closely related to SARS-CoV-2 contains natural insertions at the S1/S2 cleavage site of the spike protein. Hong Zhou, Xing Chen, Tao Hu, Juan Li, Hao Song, Yanran Liu, Peihan Wang, Di Liu, Jing Yang, Edward C. Holmes, Alice C. Hughes, Yuhai Bi, and Weifeng Shi. June 8, 2020. 30: 2196-2203. doi: https://doi.org/10.1016/j.cub.2020.05.023
aRxiv. The bat coronavirus RmYN02 is characterized by a 6-nucleotide deletion at the S1/S2 junction, and its claimed PAA insertion is highly doubtful. Yuri Deigin and Rossana Segreto. December 1, 2020.
Zenodo. Unusual features of the SARS-CoV-2 genome suggesting sophisticated laboratory modification rather than natural evolution and delineation of its probable synthetic route. Li-Meng Yan, Shu Kang, Jie Guan, and Shanchang Hu. September 14, 2020. doi: 10.5281/zenodo.4028829
Johns Hopkins Center for Health Security. In Response: Yan et al Preprint Examinations of the Origin of SARS-CoV-2. Kelsey Lane Warmbrod, Rachel M. West, Nancy D. Connell and Gigi Kwik Gronvall. September 21, 2020.
Zenodo. Proposed SARS-CoV-2 Spillover During 2019 Review of Samples from a Mineshaft in Mojiang, Yunnan Province, China. Anonymous. September 14, 2020. doi: 10.5281/zenodo.4029544
ResearchGate. An investigation into the WIV databases that were taken offline. Billy Bostickson et al. February 2021.
ResearchGate. Wuhan Institute of Biological Products Co. Rodolphe de Maistre, Gilles Demaneuf and Billy Bostickson. March 2021.
Zenodo. 1. Proposed Forensic Investigation of Wuhan Laboratories. Billy Bostickson and Yvette Ghannam. March 2021. DOI: 10.5281/zenodo.4640383
ResearchGate. 2. Investigation of RaTG13 and the 7896 Clade. Billy Bostickson and Yvette Ghannam. March 2021. DOI: 10.13140/RG.2.2.22382.33607
ResearchGate. 3. Wuhan Laboratories, Bat Research and Biosafety. Billy Bostickson and Yvette Ghannam. April 2021. DOI: 10.13140/RG.2.2.32006.29761
***
Hesari-tyhmentymän Aamukakka-lehtikin lopulta ottaa lusikan kauniiseen käteen, että todisteet koroviruksen luonnollisesta alkuperästä ovat ehdottomat, eikä Dalgleishin ja Sörensenin eikä muitakaan "keinotekoituusteorioita" enää selvitellä. Lainaus jutusta:
" *** Toki on myös muita teorioita. Esimerkiksi se, että karkuun päässyt virus olisi itse valmistettu kiinalaislaboratoriossa. Kiinassa taas on esitetty, että virus olisi valmistettu eräässä Yhdysvalloissa sijaitsevassa biolaboratoriossa. Nämä salaliittoteoriat voidaan jättää huomioimatta. *** "
Nyt vaaditaan tutkittavaksi viruksen etenemisREITTIÄ luonnosta ihmiskunnan pandemiaksi. Siinä asiassa pelataan tiedolla, jota ei voida ehdottomasti todistaa todeksi tai epätodeksi kuten itse viruksen alkuperä. Jotkut trooppiset lepakot vaivat lentää vaikka maapallom ympäri monsuunituulten mukana ja tartuttaa viruksiaan myös aivan muihin nisäkäsryhmiin.
https://www.aamulehti.fi/ulkomaat/art-2000009452421.html
" Vieläkin kiistellään, mistä miljoonia tappanut koronapandemia sai alkunsa – Tällä hetkellä vastakkain ovat nämä kaksi teoriaa
Koronaviruksen aiheuttama covid-19-tauti julistettiin pandemiaksi kolme vuotta sitten, mutta vieläkin kiistellään siitä, mistä miljoonia ihmisiä surmannut virus sai alkunsa.

Japanissa maanantaista alkaen maskia ei ole tarvinnut enää käyttää esimerkiksi julkisissa liikennevälineissä muutoin kuin ruuhka-aikoina. Moni jatkoi maskin käyttöä siitä huolimatta myös kadulla. Kuva: Kim Kyung Koon / Reuters
Vesa Vanhakakka
5:00
Aamulehti
Yhdysvaltain edustajainhuoneessa koettiin harvinainen yhtenäisyyden hetki viime perjantaina, kun demokraatit ja republikaanit äänestivät yksimielisesti äänin 419-0 sen puolesta, että maan kansallinen tiedustelu (DNI) avaisi salaista tiedustelutietoa koronapandemian aiheuttaneen sars-CoV-2-viruksen alkuperästä.
DNI on Yhdysvaltain johtava turvallisuuselin, ja tiedusteluelimet toimivat sen alaisuudessa. DNI on myös presidentin lähin neuvonantaja tiedustelukysymyksissä.
Senaatin päätöksen jälkeen presidentti Joe Biden kertoi tiedotusvälineille, että hän ei ole vielä päättänyt allekirjoittaako hän päätöksen.
Keskustelu sars-CoV-2-viruksen alkuperästä putkahti taas julkisuuteen pari viikkoa sitten, kun liittovaltion poliisin FBI:n johtaja Christopher Wray sanoi Fox News -kanavan haastattelussa, että pandemiavirus olisi saanut alkunsa Wuhanissa Kiinassa sijaitsevassa laboratoriossa tapahtuneesta onnettomuudesta.
Wray kommentoi asiaa sen jälkeen, kun Yhdysvaltain energiaministeriö oli muutamaa päivää aikaisemmin todennut, että virus oli ”todennäköisesti” päässyt karkuun Wuhanin virologisesta instituutista. Instituutti sijaitsee vajaan tunnin ajomatkan päässä wuhanilaisesta torista, mistä tartuntojen on epäilty lähteneen liikkeelle.
Yhdysvalloissa viruksen alkuperää on tutkinut kahdeksan eri viraston tiedusteluelintä, ja ne ovat kovin erimielisiä. Yksikään ei ole asiasta varma. Neljä uskoo alkuperän olevan luonnossa. Kahdella ei ole edes kantaa asiaan. Myös todennäköisyyden aste vaihtelee.
Samaan aikaan iso osa maailman tiedeyhteisöstä on sitä mieltä, että tähän asti kerätty tieto viruksesta viittaa siihen, että viruksen alkuperä on luonnossa. Tosin sataprosenttisen varmaksi tätäkään ei ole vielä osoitettu, vaikka viruksen perimää on sekvensoitu laboratorioissa miljoonia kertoja.
Kaksi teoriaa
Vastakkain on kaksi teoriaa.
Toisen mukaan virus olisi peräisin luonnosta elävästä eläimestä, jossa se on muuntunut ja siirtynyt sen jälkeen väli-isännän kautta ihmiseen.
Teoriaa tukevia todisteita on kerätty muun muassa ihmisestä toiseen levinneiden virusvarianttien geenisekvensseistä, joita on verrattu muun muassa lepakoiden ja muiden eläinten geenijaksoihin siellä, mistä pandemian uskotaan saaneen alkunsa.
Toisen teorian mukaan laboratoriossa säilytettyä luonnossa esiintyvää koronavirusta olisi jostain syystä päässyt karkuun Wuhanissa sijaitsevasta laboratoriosta.
*** Toki on myös muita teorioita. Esimerkiksi se, että karkuun päässyt virus olisi itse valmistettu kiinalaislaboratoriossa. Kiinassa taas on esitetty, että virus olisi valmistettu eräässä Yhdysvalloissa sijaitsevassa biolaboratoriossa. Nämä salaliittoteoriat voidaan jättää huomioimatta. ***
Teoria viruksen karkaamisesta Wuhanin laboratoriosta sai alkunsa Yhdysvalloissa medialle 2021 vuodetusta tiedusteluraportista, jossa väitettiin usean Wuhanin laboratorion työntekijän joutuneen sairaalahoitoon marraskuussa 2019, vain kuukautta ennen kuin virus alkoi toden teolla levitä alueella.
Maailman terveysjärjestön ryhmä sai Kiinalta luvan vierailla Wuhanin laboratoriossa 2021. Matkan jälkeisessä raportissa todettiin laboratoriovuodon olevan ”äärimmäisen epätodennäköinen”.
WHO:n raporttia on arvosteltu puutteelliseksi ja vajain tiedoin tehdyksi. Jopa WHO:n pääjohtaja Tedros Adnahom Ghebreyesus on perännyt uutta tutkimusta sanoen ”kaikkien hypoteesien olevan avoimia ja vaativan lisätutkimuksia”.
Tärkeätä selvittää
Viruksen alkuperän selvittäminen on tärkeätä monesta syystä. Virus on aiheuttanut jo lähes seitsemän miljoonaa kuolemaa ja sairastuttanut lähes 700 miljoonaa ihmistä.
[RJK: VIRUKSEN alkuperä on selvitetty! Tutkittavana on PANDEAMIAN SYNTYTAPA. Virus on saattanut ennekin levitä ihmisiinkin, mutta ei ole ennen aiheuttanut pandemiaa.]
WHO:n johtaja Ghebreyesus tviittasi lauantaina, että viruksen alkuperän ja eri hypoteesien tutkiminen on moraalisesti tärkeätä kaikkien niiden ihmisten takia, jotka ovat kuolleet koronaan tai jotka kärsivät pitkittyneestä koronataudista (long covid). Twiitin julkaisupäivänä oli kulunut kolme vuotta siitä, kun WHO nimitti epidemiaa ensimmäisen kerran pandemiaksi.
Väestössä yhä kiertävä sars-Cov-2 on vasta evoluutionsa alkuvaiheessa. Nopeasti muuntuva virus saattaa vielä tuottaa nykyistä vaarallisempia variantteja. Tieto siitä, miten virus sai alkunsa, auttaisi tulevien pandemioiden ehkäisemisessä.
Jos sars-Cov-2-viruksen alkuperäinen reitti eläimestä väli-isännän kautta ihmiseen saadaan selville, se auttaa tunnistamaan riskialueita ja lisäämään virusmuunnosten seurantaa ja kohentamaan valvontajärjestelmiä näillä alueilla.
Vaikutukset saattavat ulottua rakentamiseen, maankäyttöön, maatalouteen ja villieläinten hyödyntämiseen alueilla, missä ihminen on tunkeutunut liian lähelle eläinten maailmaa.
Vaikutukset saattavat näkyä myös elintarvikkeiden liikkumisessa maailmalla. Yksi Kiinassa esitetty teoria väittää koronaviruksen tulleen Wuhaniin toisaalta Kiinasta tai ulkomailta tuotujen lihapakasteiden mukana.
Se, karkasiko virus wuhanilaisesta laboratoriosta tai onko Kiina salannut jotain muuta olennaista tietoa koronan alkuperästä, vaikuttaa myös siihen, miten Kiinaan suhtaudutaan maailmalla. Maailmassa on jännitteitä tällä hetkellä riittävästi ilman pandemian alkuun liittyviä kyräilyä ja epävarmuuksia. Myös siksi pandemiaviruksen alkuperä on hyvä selvittää. "
***
https://www.facebook.com/watch/live/?ref=notif&v=221513643890535¬if_id=1680940868696587¬if_t=live_video_explicit
Risto Koivula
Ja mitä sellaiseen "ideaan" tulee, että NOITA ELÄINKUNNAN VIRUKSIA EI SAISI LAINKAAN TUTKIA MISSÄÄN - se nyt ainakin olisi aivan täysin perseestä!
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Risto Koivula tuota ekaa kommenttiasi en ymmärtänyt. Mutta olet sitä mieltä, että on OK kehitellä viruksista vaarallisempia ihmiselle? Eli otetaan jokin virus luonnosta joka leviää ilmateitse ja lisätään sille kyky tunkeutua ihmissoluihin jota sillä luonnollisesti ei ole?
Se virus ei nyt vaan ole mistään tutkimuksesta lähtöisin. Mikä tässä on epäselvää?
Muka "keinotekoisen tappavan osan viruksessa" (furin clavage site FCS) lörötyksen panivat liikkeelle kaksi vilttiketjun tiedehuijaria ja NATO:n disinformaattoria Angus Dalgleish ja Birger Sörensen, ja SE ON AIVAN TOTAALISTA FUULAA ja osoittaa myös, että nuo hörhövaarit eivät tienneet mitään virologiassa muualla maailmassa tapahtuneesta edistyksestä.
Ja se on justiin tuo "teoria", että sinne muka olisi kehitelty "keinotekoinen ja luonnossa mahdoton piikki" juuri ihmoissoluun tunkeutumiseksi. Se on puhdasta paskaa:
Täällä on lainattu tuota minukin referoimaani Wun ja Zhaon artikkelia.
He ovat kaksi syövän virusinfektioteorian "veteraania", jotka saivat AIDS-viruksesta ansiotonta jälkikäteistä nostetta, ja lisää tutkimusrahaa, kun ilmenee virus, joka ainakin ALTISTAA SYÖVILLE, vaikka EI OLEKAAN NIIDEN SYY.
Idean tuollaisesta "tutkimustarpeesta" olivat esittäneet USA:lainen Columbian yliopistoon liittyvän yksityosen synapsitutkimuslaitoksen johtaja Neil L Harrison ja aivan muun alan mies Jeffrey D. Sachs, jotka muuten epäilivät nimenomaan USA:n Okalamoman yliopistoa. En tiedä, onko tämä se sama mies (jolle Suomi maksoi palkkaa, kun hän suunnitteli ja valmisteli Jeltsinin Venäjän talouden lopullista tuhoamista ja kaappausta):
NATOn disinformaatio-hörhövaarit vastasisvat tähän "haasteeseen".
Viruksia ja muita mikrobeja on erittäoin vaikeaa kehittää labrassa VAARALLISEMMIKSI, mutta sen sijaan verraten HELPPO HEIKENTÄÄ ja usein niin, että sen immutettinaiheuttajaominaisuudet säilyvät. Tälle ominaisuudelle perustui ensialkuun lähes kaikki rokotekehitys. Esimerkiksi on voitu rokottaa tapettua taudinaiheuttajaa, tai sitten sen luonnossa esiintyvää lähisukulaista (lehmärokkoa isorokon torjumiseksi), joka ei sairastuta tai ainakaan tapa ihmistä.
Tässä on syytä huomata, että virus tai muu basislisko, joka varmasti tappaa, harvemmin aiheuttaa epidemiaa. Epidemianaiheuttajan pitää pystyä myös leviämään. Siihenkin ne ovat kyllä "keksineet keinoja" - esimerkiksi että tartunta voi tapahtua vain eri lajien välillä, kuten pilkkukuume ihmisen ja täin välillä.
Merkittävä seikka on myös Big Pharman ote tiedejulkaisuista. Heti kun Faucille selvisi, että vuoto heidän rahoittamasta tutkimuksesta oli selviö, hän maksoi tutkimusjulkaisun joka toitotti, ettei virus voinut olla muokattu, vaikka itse sen olivat luoneet. Eli piikkiproteiinin lisääminen lepakkojen koronavirukseen, toisin sanoin "gain a function" tutkimusta. Tätä yhtä julkaisua joka kielsi viruksen alkuperän olevan labrasta, levitettiin joka mediaan ja jopa tiedejulkaisut yhtenä suuna vannoivat sen nimeen. Jo silloin 2020 keväällä tuli sellainen tunne, että nyt on kusetuksen makua tässä asiassa. Ei tiede noin toimi, että on yksi ja ainut totuus eikä sen paikkansa pitävyyttä saa epäillä.
Risto Koivula: MITÄÄN SELLAISTA PIIKKIPROTEIINIA MIHINKÄÄN LEPAKKOJEN KORONAVIRUKSEEN EI OLE LISÄTTY.
https://www.pnas.org/doi/10.1073/pnas.2211107119
" SARS-CoV-2 furin cleavage site was not engineered
September 29, 2022
119 (40) e2211107119
Harrison and Sachs (1) make a serious accusation against scientists at the Universi-ty of North Carolina (UNC) and the Wuhan Institute of Virology (WIV) based on an eight-amino-acid sequence similarity between the furin cleavage site (FCS) of se-vere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Spike and one of the FCSs of human amiloride-sensitive epithelial sodium channel α subunit (ENaC) (2). Both proteins have the sequence RRARSVAS (Fig.1A).Harrison and Sachs cite work on rat ENaC from UNC (3, 4) and suggest that the UNC and WIV coronavirologists may have mimicked human ENaC FCS to make SARS-CoV-2 more infectious for lung epithelia.
Numerous features of SARS-CoV-2 FCS demonstrate that it was not engineered to mimic human ENaC:
• Alignment of the nucleotide sequence of the SARS-CoV-2 Spike gene with the closest known coronavirus Spike gene from Laotian bat coronavirus BANAL-20-52 (5) clearly shows that four extra amino acids (PRRA), not eight, were added to the SARS-CoV-2 Spike protein (Fig. 1B).
• There was an insertion of 12 nucleotides into the Spike gene (Fig. 1B, box) (6). This nucleotide insertion is out of frame (6, 7).
• The insertion adds a proline not present in ENaC.
• Except for one codon (cgu that encodes arginine 685), each of the codons for RRARSVAS is different in human ENaC and SARS-CoV-2 (Fig. 1B).
• Five of eight amino acids (RSVAS; underlined in Fig. 1A, red box in Fig. 1C) in or near the ENaC FCS sequence shared with SARS-Cov-2 Spike are present in Spikes of sarbecoviruses, such as BANAL-20-52. It would be illogical to use the FCS from ENac rather than from a FCS of another coronavirus.
Harrison and Sachs’s (1) claim that alignment of sarbecovirus Spike amino acid sequences illustrates“the unusual nature of the [SARS-CoV-2] FCS” is misleading. FCSs are common in coronaviruses, and present in representatives of four out of five betacoronavirus subgenuses (8). The highly variable nature of the S1/S2 junction is easily ascertained by inspecting a precise alignment of sarbecovirus Spikes (Fig. 1C).
After commenting about the “unusual nature” of the SARS-CoV-2 FCS, Harrison and Sachs (1) then argue the opposite. With regard to our earlier publication (7), they write, “In fact, the assertion that the FCS in SARS-CoV-2 has an unusual, nonstan-dard amino acid sequence is false.” We made no such assertion. Rather, we noted that the SARS-CoV-2 FCS is “suboptimal.” We also noted, correctly, that placing the insertion out of frame would be “an unusual and needlessly complex feat of genetic engineering.”
The immediate proximal ancestor of SARS-CoV-2 did not come directly from a bat to a human, but first evolved in an intermediate host. Two related lineages of SARS-CoV-2 — lineage A and lineage B — first infected humans via the wildlife trade at the Huanan Market in Wuhan (9, 10). For the ENaC hypothesis to be true, UNC or WIV researchers would have had to possess the direct SARS-CoV-2 progenitor isolated from another animal — not a bat.
Harrison and Sachs (1) allege that scientists at NIH and elsewhere, including myself and colleagues, conspired to suppress theories of a laboratory origin of SARS-CoV-2. This is false. A possible laboratory origin of SARS-CoV-2 was discussed in our earlier publications (6, 7).
References
1 N. L. Harrison, J. D. Sachs, A call for an independent inquiry into the origin of the SARS-CoV-2 virus. Proc. Natl. Acad. Sci. U.S.A. 119, e2202769119 (2022).
2 P. Anand, A. Puranik, M. Aravamudan, A. J. Venkatakrishnan, V. Soundararajan, SARS-CoV-2 strategically mimics proteolytic activation of human ENaC. eLife 9, e58603 (2020).
3 A. García-Caballero, Y. Dang, H. He, M. J. Stutts, ENaC proteolytic regulation by channel-activating protease 2. J. Gen. Physiol. 132, 521–535 (2008).
4 P. Kota, M. Gentzsch, Y. L. Dang, R. C. Boucher, M. J. Stutts, The N terminus of α-ENaC mediates ENaC cleavage and activation by furin. J. Gen. Physiol. 150, 1179 – 1187 (2018).
5 S. Temmam et al., Bat coronaviruses related to SARS-CoV-2 and infectious for human cells. Nature 604, 330–336 (2022).
6 K. G. Andersen, A. Rambaut, W. I. Lipkin, E. C. Holmes, R. F. Garry, The proximal origin of SARS-CoV-2. Nat. Med. 26, 450–452 (2020).
7 E. C. Holmes et al., The origins of SARS-CoV-2: A critical review. Cell 184, 4848–4856 (2021).
9 J. E. Pekar et al., The molecular epidemiology of multiple zoonotic origins of SARS-CoV-2. Science 377, 960–966 (2022).
10 M. Worobey et al., The Huanan Seafood Wholesale Market in Wuhan was the early epicenter of the COVID-19 pandemic. Science 377, 951–959 (2022).
***
https://healthfeedback.org/claimreview/financial-analyst-david-martin-misrepresents-studies-patent-applications-promote-baseless-claim-sars-cov-2-developed-bioweapon/
" Financial analyst David Martin misrepresents studies and patent applications to promote the baseless claim that SARS-CoV-2 was developed as a bioweapon
CLAIM
“SARS is the research developed by humans, weaponizing a life system model to actually attack human beings”
CLAIM
“SARS is the research developed by humans, weaponizing a life system model to actually attack human beings”
VERDICT
DETAILS
Misleading: Contrary to Martin’s claims, early research on coronaviruses didn’t involve modified viruses nor human experimentation apart from studies of infections with naturally-occurring human coronaviruses establishing that these viruses caused colds.
Factually inaccurate: Old patent applications for coronavirus vaccines and vectors cited by Martin are for animal coronaviruses. None of them is related to SARS-CoV-2 nor do they prove that the virus was developed as a bioweapon.
KEY TAKE AWAY
At the moment, investigations are still underway to determine where SARS-CoV-2 originated and how it came to infect humans. Both the natural and lab leak hypotheses rely on circumstantial evidence that can’t prove nor disprove either theory. However, no credible evidence indicates that the virus was engineered. Based on prior disease outbreaks, the most likely hypothesis is that SARS-CoV-2 arose naturally and that zoonotic infections were the reason for the spread of the virus in humans.
FULL CLAIM: “SARS is the research developed by humans, weaponizing a life system model to actually attack human beings, and they patented it in 2002.”; “The intent was to get the world to accept a universal vaccine template, and the intent was to use coronavirus to get there”
REVIEW
In May 2023, a video featuring financial analyst David Martin went viral on social media platforms, gathering millions of views on Facebook, Instagram, Twitter, and TikTok (examples here, here, here, and here). In it, Martin claimed that SARS-CoV-2 was an act of “premeditated domestic terrorism” and that the virus is a weapon that was engineered through decades of research with the objective of “get[ting] the world to accept a universal vaccine template”.
Martin’s 21-minute speech was only the beginning of a nine-hour event called “Inter-national COVID-19 Summit III” that was held in a room of the European Parliament in Brussels on 3 May 2023. As featured speakers, the event gathered a group of well-known COVID-19 misinformation actors, including Robert Malone, Ryan Cole, Byram Bridle, Christian Perronne, and Pierre Kory, president of the fringe medical group Front Line COVID-19 Critical Care Alliance (FLCCC).
A three-part video recording of the event was uploaded on Rumble, nd video excerpts were widely spread online, aided by anti-vaccine, COVID-19 skeptic, and conspiracy groups and individuals who shared them. Among all the speakers, Martin’s speech attracted much attention online, receiving shares from FLCCC, the conspiracy website Infowars, and the anti-vaccine group Children’s Health Defense, as well as many social media users.
However, Martin’s claims are all unsubstantiated, contain numerous inaccuracies, and are based on a grossly distorted interpretation of historical coronavirus research that we will analyze in detail below.
The place where the summit took place and the summit’s use of the European Parliament’s logo was also misleading, lending a veneer of legitimacy to claims that the speakers had testified to the European Parliament. However, this wasn’t the case. Firstly, the event doesn’t appear in the list of official events on the European Parliament website.
Secondly, the event wasn’t held at the Hemicycle, where the 705 Members of the European Parliament (MEPs) gather during plenary sessions. Instead, it took place in one of the rooms available to MEPs, which was possible because the Summit was hosted by five MEPs, Cristian Terhes, Christine Anderson, Ivan Vilibor Sinčić, Francesca Donato, and Mislav Kolakušić, all of them known COVID-19 skeptics.
Thirdly, the European assembly clearly explained to CheckNews—a fact-checking section of the French newspaper Libération—that the European Parliament “didn’t organize or finance” this event, although some MEPs took part, “exercising their freedom of mandate”.
Claim 1 (Inaccurate and Misleading):
“coronavirus as a model of a pathogen was isolated in 1965. Coronavirus was identified in 1965 as one of the first infectious replicatable [sic] viral models that could be used to modify a series of other experiences of human condition.”
While it is unclear what Martin meant with “a model of pathogen”, the first corona-virus wasn’t isolated in 1965 but in 1936. That year, Beach and Schalm isolated the pathogen that caused avian bronchitis in newborn chickens, which symptoms had been described five years earlier, and determined that the disease was caused by a virus [1].
It still took 30 years to identify the first human coronavirus, 229E, discovered by Do-rothy Hamre at the University of Chicago in 1962 when she analyzed tissue cultures of students with colds[2]. Around the same time, two research teams, one led by Da-vid Tyrrell in England and another by Ken McInstosh in the U.S., independently iso-lated two additional human coronaviruses, called B814 and OC43, respectively [3,4].
However, Martin’s claim that these viruses were immediately identified as a modifiable model is unsubstantiated because at that time, scientists didn’t know that they belonged to the same family. The term coronavirus was only introduced in 1968 when Tyrrell and June Almeida observed the viruses under the electron microscope and found that they all had their surface covered with characteristic spikes that resembled the sun’s corona.
Claim 2 (Inaccurate and Misleading):
“in 1966, the very first COV coronavirus model was used as a transatlantic biological experiment in human manipulation”; “And in 1967, the year I was born, we did the first human trials on inoculating people with modified coronavirus”
Martin accompanied these allegations with several scientific references. However, none of the studies he cited support such claims.
The first of those studies was conducted at the U.S. National Institutes of Health (NIH) and published in 1967—not in 1966, as Martin claimed. In it, McIntosh and colleagues collected nasopharyngeal fluid from NIH employees who had cold symptoms, isolated the viruses in them, and grew these viruses in laboratory cells and tissues[4].
The second study, published by Almeida and Tyrell also in 1967,described a method for detecting viral particles in organ cultures by electron microscopy. The authors observed that the recently identified 229E and B814 viruses were “morphologically identical” to the one that caused avian infectious bronchitis [5].
Finally, Martin cited a third study published by Bradburne, Bynoe, and Tyrell in 1967. This study is the only one that used human volunteers, who were inoculated with Hamre’s 229E virus isolates. The researchers observed that 13 of the 26 inoculated volunteers developed colds, providing the first experimental evidence that the new virus caused this condition[6].
From the information above, it is clear that Martin’s description is quite misleading, and these experiments can hardly be considered “a transatlantic biological experi-ment in human manipulation”. Furthermore, the claim is also inaccurate because none of these studies involved manipulated viruses.
Health Feedback tried to reach out to Martin for comment through the “Contact Us” section of his company’s (M-MCAM International) website, but the link was unresponsive. We will update this review if new information becomes available.
Claim 3 (Incorrect):
“Ironically, the common cold was turned into a chimera in the 1970s. And in 1975, 1976, and 1977, we started figuring out how to modify coronavirus by putting it into different animals, pigs and dogs.”
This claim demonstrates a gross misunderstanding of what coronaviruses are because it seems to suggest that there is only one coronavirus, that it can only cause colds, and that the only way it can get into animals is by “putting” it there. However, all these implications are incorrect.
The reference Martin cited to support his claim doesn’t show any human manipula-tion of coronaviruses. On the contrary, it is a 1992 study that used an unmodified rabbit coronavirus occurring in nature to model the disease in rabbits[7]. The resear-chers isolated the virus from moribund animals and injected it intravenously or intra-muscularly in laboratory rabbits, observing that it caused myocarditis. This simple study found that coronavirus infection in rabbits might progress into heart muscle problems.
It is important to note that the term coronavirus doesn’t refer to a single virus as Martin seemed to suggest, but to a large family of viruses comprising more than 40 different viruses. Some of these viruses are specialized in infecting humans, while others specifically target a particular animal, such as dogs, cats, birds, or pigs. While coronavirus infections in humans primarily result in respiratory diseases, in other animals like pigs or dogs, they can cause gastroenteritis or other symptoms.
Hence, there is no link between SARS-CoV-2 and these animal coronaviruses because they are different viruses, each one with different characteristics that aren’t interchangeable.
Claim 4 (Incorrect):
“As a matter of fact, every publication on vaccines for coronavirus from 1990 until 2018, every single publication concluded that coronavirus escapes the vaccine impulse because it modifies and mutates too quickly for vaccines to be effective”
Martin’s claim is false because effective vaccines against coronaviruses were available years before the COVID-19 pandemic for several conditions affecting pets and livestock, as the U.K. Royal Society of Biology explains.
Ian Frazer, an immunologist and emeritus professor at the University of Queensland, told ABC News in 2020 that developing a vaccine against human coronaviruses is so challenging partly because the virus infects the upper respiratory tract. The problem is that the immune system isn’t particularly effective in this region, which means that a response induced by a vaccine will likely miss the target cells.
Claim 5 (Inaccurate):
“Dog breeders and pig farmers found that coronavirus created gastrointestinal problems, and that became the basis for Pfizer’s first Spike protein vaccine patent filed”; in 2002, the University of North Carolina Chapel Hill patented “an infectious replication defective clone of coronavirus […] Infectious replication defective means a weapon. It means something meant to target an individual but not have collateral damage to other individuals”
Searching patent databases for old applications containing the word coronavirus has proven a prolific source of conspiracy theories, all claiming to have found the smo-king gun that the COVID-19 pandemic was planned or SARS-CoV-2 engineered. But as the McGill University’s Office for Science in Society explained in this article, none of these claims have any basis because those patents are unrelated to SARS-CoV-2.
Like many earlier such claims, Martin cited a patent application filed by Pfizer for “the very first spike protein vaccine for coronavirus” in 1990. Indeed, a patent (WO1993023422A1) protected the development of the first vaccine specifically tar-geting a coronavirus spike protein. However, this patent didn’t involve SARS-CoV-2 or any other human coronavirus. Instead, it targeted a cat coronavirus that caused highly lethal peritonitis in these animals.
Therefore, neither the specific patent nor the general strategy of targeting the spike protein—unsurprising considering that the spike protein forms the distinctive feature of the coronavirus family—suggest in any way that the SARS-CoV-2 virus was engineered, as Martin claimed.
Martin also cited another patent (WO02086068A2),submitted in this case by the Uni- versity of North Carolina at Chapel Hill in 2002. Pointing out that this patent “myste-riously preceded SARS 1.0 by a year”, Martin suggested that this research could be the origin of not only SARS-CoV-2 but even the SARS-CoV-1 epidemic. He went even further by claiming that a term included in the patent, “infectious replication-defective clone”, means that the new virus is “a weapon” designed to target certain individuals. This is false.
Replication-defective means that portions of the viral genome essential for forming new viral copies have been removed, resulting in a viral vector that can no longer replicate. These replication-defective viruses are often used to introduce genetic material of interest into target cells by inserting it in the space left by the removal of the replication genes.
Martin wasn’t the first one to point at the patent of the University of North Carolina at Chapel Hill as evidence that SARS-CoV-2 is a bioweapon. But this claim is funda-mentally baseless because the patent in question is entirely unrelated to SARS-CoV-2 and refers to a coronavirus that causes gastroenteritis in pigs.
Conclusion
In summary, Martin’s speech doesn’t provide the smoking gun for COVID-19 origin that he and others claimed to be.The alleged evidence presented is nothing but a list of misrepresented studies on early coronavirus research and old patent applications on animal coronaviruses all unrelated to SARS-CoV-2 or the COVID-19 pandemic.
None of the cited studies and patents suggests that the virus was engineered.In fact, some of Martin’s claims aren’t even new and have already been debunked. While there are still questions about whether the virus SARS-CoV-2 had infected humans through a naturally-occurring spillover event or a lab leak incident, there is simply no evidence to suggest that SARS-CoV-2 was developed as a bioweapon.
REFERENCES
Coronavirus SARS-CoV-2
Published on: 07 Jun 2023 | Editor: Iria Carballo-Carbajal
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Tähän tuli iso lisäys pelkästään MH17:sta heinäkuussa 2014

List of Dead Microbiologists:
The worlds top anti-virus microbiologists are being killed off. By 2005, 40 were dead. Today, over 100. Many murdered, the rest died under very suspicious circumstances. It is known they were all working on highly sensitive or government-funded research projects tied to bio-weapons and viral pandemics.
Are these silenced ‘whistleblowers’ who knew too much?
Why isn’t the mainstream media report in on this story?
Died 2006
#80: Lee Jong-woo, age 61. Died: May 22, 2006 after suffering a blood clot on the brain. Lee was spearheading the organization’s fight against global threats from bird flu, AIDS and other infectious diseases. WHO director-general since 2003, Lee was his country’s top international official. The affable South Korean, who liked to lighten his press conferences with jokes, was a keen sportsman with no history of ill-health, according to officials.Died 2005
#79: Leonid Strachunsky. Died: June 8, 2005 after being hit on the head with a champagne bottle. Strachunsky specialized in creating microbes resistant to biological weapons. Strachunsky was found dead in his hotel room in Moscow, where hed come from Smolensk en route to the United States. Investigators are looking for a connection between the murder of this leading bio weapons researcher and the hepatitis outbreak in Tver, Russia.
#78: Robert J. Lull, age 66. Died: May 19, 2005 of multiple stab wounds. Despite his missing car and apparent credit card theft, homicide Inspector Holly Pera said investigators aren’t convinced that robbery was the sole motive for Lull’s killing. She said a robber would typically have taken more valuables from Lull’s home than what the killer left with. Lull had been chief of nuclear medicine at San Francisco General Hospital since 1990 and served as a radiology professor at UCSF. He was past president of the American College of Nuclear Physicians and the San Francisco Medical Society and served as editor of the medical society’s journal, San Francisco Medicine, from 1997 to 1999. Lee Lull said her former husband was a proponent of nuclear power and loved to debate his political positions with others.
#77: Todd Kauppila, age 41. Died: May 8, 2005 of hemorrhagic pancreatitis at the Los Alamos hospital, according to the state medical examiner’s office. Picture of him was not available to due secret nature of his work. This is his funeral picture. His death came two days after Kauppila publicly rejoiced over news that the lab’s director was leaving. Kauppila was fired by director Pete Nanos on Sept. 23, 2004 following a security scandal. Kauppila said he was fired because he did not immediately return from a family vacation during a lab investigation into two classified computer disks that were thought to be missing. The apparent security breach forced Nanos to shut down the lab for several weeks. Kauppila claimed he was made a scapegoat over the disks, which investigators concluded never existed. The mistake was blamed on a clerical error. After he was fired, Kauppila accepted a job as a contractor at Bechtel Nevada Corp., a research company that works with Los Alamos and other national laboratories. He was also working on a new Scatter Reduction Grids in Megavolt Radiography focused on metal plates or crossed grids to act to stop the scattered radiation while allowing the unscattered or direct rays to pass through with other scientists: Scott Watson (LANL, DX-3), Chuck Lebeda (LANL, XTA), Alan Tubb (LANL, DX-8), and Mike Appleby (Tecomet Thermo Electron Corp.)
#76: David Banks, age 55. Died: May 8, 2005. Banks, based in North Queensland, died in an airplane crash, along with 14 others. He was known as an Agro Genius inventing the mosquito trap used for cattle. Banks was the principal scientist with quarantine authority, Biosecurity Australia, and heavily involved in protecting Australians from unwanted diseases and pests. Most of Dr Banks’ work involved preventing potentially devastating diseases making their way into Australia. He had been through Indonesia looking at the potential for foot and mouth disease to spread through the archipelago and into Australia. Other diseases he had fought to keep out of Australian livestock herds and fruit orchards include classical swine fever, Nipah virus and Japanese encephalitis.
#75: Dr. Douglas James Passaro, age 43. Died April 18, 2005 from unknown cause in Oak Park, Illinois. Dr. Passaro was a brilliant epidemiologist who wanted to unlock the secrets of a spiral-shaped bacteria that causes stomach disease. He was a professor who challenged his students with real-life exercises in bioterrorism. He was married to Dr. Sherry Nordstrom..
#74: Geetha Angara, age 43. Died: February 8, 2005. This formerly missing chemist was found in a Totowa, New Jersey water treatment plant’s tank. Angara, 43, of Holmdel, was last seen on the night of Feb. 8 doing water quality tests at the Passaic Valley Water Commission plant in Totowa, where she worked for 12 years. Divers found her body in a 35-foot-deep sump opening at the bottom of one of the emptied tanks. Investigators are treating Angara’s death as a possible homicide. Angara, a senior chemist with a doctorate from New York University, was married and mother of three.
#73: Jeong H. Im, age 72. Died: January 7, 2005. Korean Jeong H. Im, died of multiple stab wounds to the chest before firefighters found in his body in the trunk of a burning car on the third level of the Maryland Avenue Garage. A retired research assistant professor at the University of Missouri – Columbia and primarily a protein chemist, MUPD with the assistance of the Columbia Police Department and Columbia Fire Department are conducting a death investigation of the incident. A “person of interest” described as a male 6′–6’2″ wearing some type of mask possible a painters mask or drywall type mask was seen in the area of the Maryland Avenue Garage. Dr. Im was primarily a protein chemist and he was a researcher in the field.
Died in 2004
#72: Darwin Kenneth Vest, born April 22, 1951, was an internationally renowned entomologist, expert on hobo spiders and other poisonous spiders and snakes. Darwin disappeared in the early morning hours of June 3, 1999 while walking in downtown Idaho Falls, Idaho (USA). The family believes foul play was involved in his disappearance. A celebration of Darwin’s life was held in Idaho Falls and Moscow on the one-year anniversary of his disappearance. The services included displays of Darwin’s work and thank you letters from school children and teachers. Memories of Darwin were shared by at least a dozen speakers from around the world and concluded with the placing of roses and a memorial wreath in the Snake River. A candlelight vigil was also held that evening on the banks of the Snake River.
Darwin was declared legally dead the first week of March 2004 and now the family is in the process of obtaining restraining orders against several companies who saw fit to use his name and photos without permission. His brother David is legal conservator of the estate and his sister Rebecca is handling issues related to Eagle Rock Research and ongoing research projects.
Media help in locating Darwin is welcome. Continuing efforts to solve this mystery include recent DNA sampling. Stories about his disappearance continue to appear throughout the world. Issues surrounding missing adult investigations have received new attention following the tragedies of 911.
#'s 70-71: Tom Thorne, age 64; Beth Williams, age 53; Died: December 29, 2004. Two wild life scientists, Husband-and-wife wildlife veterinarians who were nationally prominent experts on chronic wasting disease and brucellosis were killed in a snowy-weather crash on U.S. 287 in northern Colorado.
#69: Taleb Ibrahim al-Daher. Died: December 21, 2004. Iraqi nuclear scientist was shot dead north of Baghdad by unknown gunmen. He was on his way to work at Diyala University when armed men opened fire on his car as it was crossing a bridge in Baqouba, 57 km northeast of Baghdad. The vehicle swerved off the bridge and fell into the Khrisan river. Al-Daher, who was a professor at the local university, was removed from the submerged car and rushed to Baqouba hospital where he was pronounced dead.
#68: John R. La Montagne, age 61. Died: November 2, 2004. Died while in Mexico, no cause stated, later disclosed as pulmonary embolism. PhD, Head of US Infectious Diseases unit under Tommie Thompson. Was NIAID Deputy Director. Expert in AIDS Program work and Microbiology and Infectious Diseases.
#67: Matthew Allison, age 32. Died: October 13, 2004. Fatal explosion of a car parked at an Osceola County, Fla., Wal-Mart store. It was no accident, Local 6 News has learned. Found inside a burned car. Witnesses said the man left the store at about 11 p.m. and entered his Ford Taurus car when it exploded. Investigators said they found a Duraflame log and propane canisters on the front passenger’s seat. Allison had a college degree in molecular biology and biotechnology.
#66: Mohammed Toki Hussein al-Talakani, age 40. Died: September 5, 2004: Iraqi nuclear scientist was shot dead in Mahmudiya, south of Baghdad. He was a practicing nuclear physicist since 1984.
#65: Professor John Clark, Age 52, Died: August 12, 2004. Found hanged in his holiday home. An expert in animal science and biotechnology where he developed techniques for the genetic modification of livestock; this work paved the way for the birth, in 1996, of Dolly the sheep, the first animal to have been cloned from an adult. Head of the science lab which created Dolly the sheep. Prof Clark led the Roslin Institute in Midlothian, one of the world s leading animal biotechnology research centers. He played a crucial role in creating the transgenic sheep that earned the institute worldwide fame. He was put in charge of a project to produce human proteins (which could be used in the treatment of human diseases) in sheep’s milk. Clark and his team focused their study on the production of the alpha-I-antitryps in protein, which is used for treatment of cystic fibrosis. Prof Clark also founded three spin-out firms from Roslin – PPL Therapeutics, Rosgen and Roslin BioMed.
#64: Dr. John Badwey, age 54. Died: July 21, 2004. Scientist and accidental politician when he opposed disposal of sewage waste program of exposing humans to sludge. Suddenly developed pneumonia like symptoms then died in two weeks. Biochemist at Harvard Medical School specializing in infectious diseases.
#63: Dr. Bassem al-Mudares. Died: July 21, 2004. Mutilated body was found in the city of Samarra, Iraq*. He was a Phd. chemist and had been tortured before being killed. He was a drug company worker who had a chemistry doctorate.
#62: Professor Stephen Tabet, age 42. Died on July 6, 2004 from an unknown illness. He was an associate professor and epidemiologist at the University of Washington. A world-renowned HIV doctor and researcher who worked with HIV patients in a vaccine clinical trial for the HIV Vaccine Trials Network
#61: Dr. Larry Bustard, age 53. Died July 2, 2004 from unknown causes. He was a Sandia scientist in the Department of Energy who helped develop a foam spray to clean up congressional buildings and media sites during the anthrax scare in 2001. He worked at Sandia National Laboratories in Albuquerque. As an expert in bioterrorism, his team came up with a new technology used against biological and chemical agents.
#60: Edward Hoffman, age 62. Died July 1, 2004 from unknown causes. Hoffman was a professor and a scientist who also held leadership positions within the UCLA medical community. He worked to develop the first human PET scanner in 1973 at Washington University in St. Louis.
#59: John Mullen, age 67. Died: June 29, 2004. A Nuclear physicist poisoned with a huge dose of arsenic. A nuclear research scientist with McDonnell Douglas. Police investigating will not say how Mullen was exposed to the arsenic or where it came from. At the time of his death he was doing contract work for Boeing.
#58: Dr. Paul Norman, age 52. Died: June 27, 2004. From Salisbury Wiltshire. Killed when the single-engine Cessna 206 he was piloting crashed in Devon. Expert in chemical and biological weapons. He traveled the world lecturing on defending against the scourge of weapons of mass destruction. He was married with a 14-year-old son and a 20-year-old daughter, and was the chief scientist for chemical and biological defense at the Ministry of Defense’s laboratory at Porton Down, Wiltshire. The crash site was examined by officials from the Air Accidents Investigation Branch and the wreckage of the aircraft was removed from the site to the AAIB base at Farnborough.
#57: Dr. Assefa Tulu, age 45. Died: June 24, 2004. Dr. Tulu joined the health department in 1997 and served for five years as the county’s lone epidemiologist. He was charged with trackcing the health of the county, including the spread of diseases, such as syphilis, AIDS and measles. He also designed a system for detecting a bioterrorism attack involving viruses or bacterial agents. Tulu often coordinated efforts to address major health concerns in Dallas County, such as the West Nile virus outbreaks of the past few years, and worked with the media to inform the public. Found face down, dead in his office. The Dallas County Epidemiologist died of a hemorrhagic stroke.
#56: Thomas Gold, age 84. Died: June 22, 2004. Austrian born Thomas Gold famous over the years for a variety of bold theories that flout conventional wisdom and reported in his 1998 book, “The Deep Hot Biosphere,” the idea challenges the accepted wisdom of how oil and natural gas are formed and, along the way, proposes a new theory of the beginnings of life on Earth and potentially on other planets. Long term battle with heart failure. Gold’s theory of the deep hot biosphere holds important ramifications for the possibility of life on other planets, including seemingly inhospitable planets within our own solar system. He was Professor Emeritus of Astronomy at Cornell University and was the founder (and for 20 years director) of Cornell Center for Radiophysics and Space Research. He was also involved in air accident investigations.
#55: Antonina Presnyakova, age 46. Died: May 25, 2004. A Russian scientist at a former Soviet biological weapons laboratory in Siberia died after an accident with a needle laced with ebola. Scientists and officials said the accident had raised concerns about safety and secrecy at the State Research Center of Virology and Biotechnology, known as Vector, which in Soviet times specialized in turning deadly viruses into biological weapons. Vector has been a leading recipient of aid in an American program.
#54: Dr. Eugene Mallove, age 56. Died: May 14, 2004. Autopsy confirmed Mallove died as a result of several blunt-force injuries to his head and neck. Ruled as murder. Found at the end of his driveway. Alt. Energy Expert who was working on viable energy alternative program and announcement. Norwich Free Academy graduate.Beaten to death during an alleged robbery. Mallove was well respected for his knowledge of cold fusion. He had just published an “open letter” outlining the results of and reasons for his last 15 years in the field of “new energy research.” Dr. Mallove was convinced it was only a matter of months before the world would actually see a free energy device.
#53: William T. McGuire, age 39. Found May 5, 2004, last seen late April 2004. Body found in three suitcases floating in Chesapeake Bay. He was NJ University Professor and Senior programmer analyst and adjunct professor at the New Jersey Institute of Technology in Newark. He emerged as one of the world’s leading microbiologists and an expert in developing and overseeing multiple levels of biocontainment facilities.
#52: Ilsley Ingram, age 84. Died on April 12, 2004 from unknown causes. Ingram was Director of the Supraregional Haemophilia Reference Centre and the Supraregional Centre for the Diagnosis of Bleeding Disorders at the St. Thomas Hospital in London. Although his age is most likely the reason for his death, why wasn’t this confirmed by the family in the news media?
#51: Mohammed Munim al-Izmerly, Died: April 2004. This distinguished Iraqi chemistry professor died in American custody from a sudden hit to the back of his head caused by blunt trauma. It was uncertain exactly how he died, but someone had hit him from behind, possibly with a bar or a pistol. His battered corpse turned up at Baghdad’s morgue and the cause of death was initially recorded as “brainstem compression”. It was discovered that US doctors had made a 20cm incision in his skull.
#50: Vadake Srinivasan, Died: March 13, 2004. Microbiologist crashed car into guard rail in Baton Rouge, LA. Death was ruled a stroke. He was originally from India, was one of the most-accomplished and respected industrial biologists in academia, and held two doctorate degrees.
#49: Dr. Michael Patrick Kiley, age 62. Died: January 24, 2004. Died of massive heart attack. Ebola, Mad Cow Expert, top of the line world class. It is interesting to note, he had a good heart, but it “gave out”. Dr. Shope and Dr. Kiley were working on the lab upgrade to BSL 4 at the UTMB Galvaston lab for Homeland Security. The lab would have to be secure to house some of the deadliest pathogens of tropical and emerging infectious disease as well as bioweaponized ones.
#48: LEAD Technologies Inc. V1.01 Robert Shope, age 74. Died: January 23, 2004. Virus Expert Who Warned of Epidemics, Dies died of lung transplant complications. Later purported to have died of Idiopathic Pulmonary Fibrosis which can be caused by either environmental stimulus or a VIRUS. It would not be hard to administer a drug that would cause Dr. Shope’s lung transplant to either be rejected or to cause complications from the transplant. Dr. Shope led the group of scientists who had an 11 MILLION dollar fed grant to ensure the new lab would keep in the nasty bugs. Dr. Shope also met with and worked with Dr. Mike Kiley on the UTMB Galveston lab upgrade to BSL 4. When the upgrade would be complete the lab will host the most hazardous pathogens known to man especially tropical and emerging diseases as well as bioweapons.
#47: Dr Richard Stevens, age 54. Died: January 6, 2004. He had disappeared after arriving for work on 21 July, 2003. A doctor whose disappearance sparked a national manhunt, killed himself because he could not cope with the stress of a secret affair, a coroner has ruled. He was a hematologist. (hematologists analyze the cellular composition of blood and blood producing tissues e.g. bone marrow).
Died 2003
#46: Robert Aranosia, age 61. Died: December 18, 2003. While driving south on I-75 his pickup truck went off the freeway near a bridge over the Kawkawlin River. The vehicle rolled over several times before landing in the median. Aranosia was thrown from the vehicle and ended up on the shoulder of the northbound lanes. He was the Oakland County deputy medical examiner.
#45: Robert Leslie Burghoff, age 45. Died: November 20, 2003. Scientist. Killed by a hit and run driver that jumped the curb and ploughed into him in the 1600 block of South Braeswood, Texas. The driver was described as a short Hispanic man in his 50s with a slightly rounded face. He was studying the virus plaguing cruise ships.
#44: Michael Perich, age 46. Died: October 11, 2003. Died in one-vehicle car accident. The LSU West Nile research scientist was wearing his seat belt and drowned. He was LSU professor who helped fight the spread of the West Nile virus. Perich, who was known as one of the country’s experts on vector-borne diseases, had most recently led a crusade to keep down the effects of West Nile virus and to get many of the Louisiana’s parishes to work toward forming mosquito control districts.
#43: David Kelly, age 59. Died: July 18, 2003. British biological weapons expert, was said to have slashed his own wrists while walking near his home. Kelly was the Ministry of Defense’s chief scientific officer and senior adviser to the proliferation and arms control secretariat, and to the Foreign Office’s non-proliferation department. The senior adviser on biological weapons to the UN biological weapons inspections teams (Unscom) from 1994 to 1999, he was also, in the opinion of his peers, pre-eminent in his field, not only in this country, but in the world.
#42: Dr. Leland Rickman, age 47. Died: June 24, 2003. Rickman died while on a teaching assignment in Lesotho, a small country bordered on all sides by South Africa. UC San Diego expert on infectious diseases and, since September 11, 2001 a consultant on bioterrorism. He had complained of a headache, but the cause of death was not immediately known. The physician had been working in Lesotho with Dr. Chris Mathews, director of the UC San Diego Medical Center’s Owen Clinic, teaching African medical personnel about the prevention and treatment of AIDS. Rickman, the incoming president of the Infectious Disease Assn. of California, was a multidisciplinary professor and practitioner with expertise in infectious diseases, internal medicine, epidemiology, microbiology and antibiotic utilization.
#41: ‘Dr. Roger’ Died: Summer 2003. ‘Roger’ was pseudonym for this genetics scientist. He was 17 and lived in Roswell, New Mexico in 1947 when the unexplained object crashed. He told a woman he worked with in 1977 named ‘Kate’ while employed by the Navy, who he helped to clean up the crash site of the 1947 UFO. He subsequently went to work for the government at this young age and ended up a geneticist working in China Lake for the Navy. Although he lived in fear and hiding soon after he told his story to Kate, he retired in late 1990s or early 2000′s and she saw him again once in early 2002 in San Diego. He told her she was in danger to talk to him and he left the store. In 2003 she received a phone call from his ‘friend’ who said he had been executed in his retirement home in Connecticut. The body had been removed by a black government looking vehicle. The home had been cleaned up and the body removed without any public notices of his death or existence. Many disfigured and abnormal animals were found in the desert near Groom Lake during his time there and after. Kate thought he might have been doing this gruesome experimental work.
#40: Carlo Urbani, age 46. Died: in April 2003 in Bangkok from SARS (severe acute respiratory syndrome) – the new disease that he had helped to identify. Thanks to his prompt action, the epidemic was contained in Vietnam. However, because of close daily contact with SARS patients, he contracted the infection. On March 11, he was admitted to a hospital in Bangkok and isolated. Less than three weeks later he died. He was a dedicated and internationally respected Italian epidemiologist, who did work of enduring value combating infectious illness around the world.
Died 2002
#39: Roman Kuzmin. Died December 2002. A 24-year-old Russian surgeon studying in Connecticut was fatally struck by a car as he fled a store with three stolen rolls of film, police said. He was studying to be an orthopedic surgeon. Doctors who worked with Roman Kuzmin at Waterbury Hospital said they were stunned to hear of his death Sunday evening and many couldn’t believe the circumstances. Kuzmin left Vladivostok in September to study orthopedic surgical techniques at Waterbury Hospital under a Keggi Othopedic Foundation program. Dr. Kristaps Keggi, who organized the program, said Kuzmin was “very able, very bright – a superb student and a superb individual.”
#38 B: Dr. David R. Knibbs, age 49. Died: August 5, 2002. Respected pathobiologist specializing in electron microscopy.
#38: Steven Mostow, age 63. Died: March 25, 2002. One of the country’s leading infectious disease and bioterrorism experts and was associate dean at the University of Colorado Health Sciences Center. He died in a plane crash near Centennial Airport. He was known as “Dr. Flu” for his expertise in treating influenza, and expertise on bioterrorism. Mostow was one of the country’s leading infectious disease experts.
#37: Dr. David Wynn-Williams, age 55. Died: March 24, 2002. Hit by a car while jogging near his home in Cambridge, England. He was an astrobiologist with the Antarctic Astrobiology Project and the NASA Ames Research Center. He was studying the capability of microbes to adapt to environmental extremes, including the bombardment of ultraviolet rays and global warming.
#35-36: Tanya Holzmayer, age 46, Died: February 28, 2002: Two dead microbiologists in San Francisco. While taking delivery of a pizza, Tanya Holzmayer was shot and killed by a colleague,
Guyang “Mathew” Huang, 38, who then apparently shot himself. Holzmayer moved to the US from Russia in 1989. Her research focused on the part of the human molecular structure that could be affected best by medicine. Holzmayer was focusing on helping create new drugs that interfere with replication of the virus that causes AIDS. One year earlier, Holzmayer obeyed senior management orders to fire Huang. Huang appeared from behind the deliveryman. He shot Holzmayer several times at close range in the chest and head. As Holzmayer fell in her doorway, Huang ran to a Ford Explorer and drove away. Less than an hour after the shooting, Huang called his wife, according to Foster City Police Capt. Craig Courtin. He told her about the shooting and that he was going to kill himself, then he hung up. Huang’s wife called the emergency services and Foster City police used search dogs to comb the area. They ran into a jogger who had seen Huang’s body lying off the walkway that locals call “The Levee.” He had fired a single bullet into his head.
#34: Dr. Ian Langford, age 40, Died: February 12, 2002. Found dead at his blood-spattered and apparently ransacked home A Russian who was a Senior Research Associate in CSERGE, UK. He was a leading university research scientist working on Global Environment, specializing in links between human health and the environment risk, was. Specialist in leukemia and infections.
#33: Dr. Vladamir ”Victor” Korshunov, age 56. Died: February 9, 2002. Found dead on a Moscow street. Head was bashed in. Korshunov was head of the microbiology sub-facility at the Russian State Medical University. He was found dead in the entrance to his home with a head injury. On Feb. 9 the Russian newspaper Pravda reported that Korshunov had probably invented a vaccine protecting from any biological arm.
#32: David W. Barry, age 58, Died: January 28, 2002. Scientist who co-discovered AZT, the antiviral drug that is considered the first effective treatment for AIDS. Circumstance of Death are unknown.
#31: Dr. Ivan Glebov. Died: January 2002. Russian Microbiologist. Glebov died as the result of a bandit attack. Well known around the world and members of the Russian Academy of Science.
#30: Dr. Alexi Brushlinski. Died: January 2002. Russian Microbiologist. Murdered in Moscow from bandit attack. Well known around the world and members of the Russian Academy of Science.
Died 2001
#29 Dr. Benito Que, age 52. Found: November 12, 2001. Died: December 6, 2001. Found Comatose from what was called a mugging. Died later in hospital. Found in the street near the laboratory where he worked at the University of Miami Medical School. Among Dr. Que’s friends and family there is firm belief that Dr. Que was attacked by four men, at least one of whom had a baseball bat. Dr. Que’s death has now been officially ruled “natural”, caused by cardiac arrest. He was a cell biologist, involved in research on aids, oncology research in the hematology department.
#28: Dr. Vladimer Pasechnik, age 64. Died: December 23, 2001. Found dead in Wiltshire, England, a village near his home. Two different dates have been reported: November 21 and December 23. Death ruled stroke. He had defected from Russia to UK. He had been the #1 scientist in the FSU’s bioweapons program. It was thought he was involved with exhuming the bodies of the 10 London victims of the 1919 Type A flu epidemic. Pasechnik died six weeks after the planned exhumations were announced. On November 23, 2001, Pasechnik’s death was reported in the New York Times as having occurred two days earlier. Pasechnik’s death was made in the United States by Dr. Christopher Davis of Virginia, who stated that the cause of death was a stroke. Dr. Davis was the member of British intelligence who de-briefed Dr. Pasechnik at the time of his defection. Pasechnik was heavily involved in DNA sequencing research. He had just founded a company like three other microbiologists working to provide powerful alternatives to antibiotics. Dr. Vladimir Pasechnik was the boss of William C. Patrick III who holds 5 patents on the militarized anthrax used by the United States. Patrick is now a private biowarfare consultant to the military and CIA. Patrick developed the process by which anthrax spores could be concentrated at the level of one trillion spores per gram. No other country has been able to get concentrations above 500 billion per gram. The anthrax that was sent around the eastern United States last fall was concentrated at one trillion spores per gram.
#27: Dr. Don Wiley, age 57. Vanished: December 16, 2001. Molecular Biologist with Howard Hughes Medical Institute, Harvard University, top Deadly Contagious Virus expert, abandoned rental car was found on the Hernando de Soto Bridge outside Memphis, TN. He was heavily involved in research on DNA sequencing, and was last seen at around midnight on November 16, leaving the St. Jude’s Children’s Research Advisory Dinner at The Peabody Hotel in Memphis, TN. Associates attending the dinner said he showed no signs of intoxication, and no one has admitted to drinking with him. Body found floating one month later. Workers at a hydroelectric plant in Louisiana found the body of Don Wiley on Thursday, about 300 miles south of where the molecular biologist was last seen on Nov. 18 at a medical meeting in Memphis. On January 14, 2002 (almost two months later) Shelby County Medical Examiner O.C. Smith announced that his department had ruled Dr. Wiley’s death to be “accidental”; the result of massive injuries suffered in a fall from the Hernando de Soto Bridge. Smith said there were paint marks on Wiley’s rental car similar to the paint used on construction signs on the bridge, and that the car’s right front hubcap was missing. There has been no report as to which construction signs Dr. Wiley hit.
#26: Dr. Set Van Nguyen, age 44. Died: December 14, 2001. Found dead in the airlock entrance to the walk-in refrigerator in the laboratory he worked at in Victoria State, Australia. The room was full of deadly gas which had leaked from a liquid nitrogen cooling system. Room was vented. Working on a vaccine to protect against biological weapons, or a weapon itself. In January, 2001, the magazineNature published information that two scientists, Dr. Ron Jackson and Dr. Ian Ramshaw, using genetic manipulation and DNA sequencing, had created an incredibly virulent form of mousepox, a cousin of smallpox and Dr. Nguyen had worked for 15 years at the same Australian facility. Now for the intriguing part of this story. On Friday, November 2nd, the Washington Post reported: ”Officials are now scrambling to determine how a quiet, 61-year-old Vietnamese immigrant, riding the subway each day to and from her job in a hospital stockroom, was exposed to the deadly anthrax spores that killed her this week. They worry because there is no obvious connection to the factors common to earlier anthrax exposures and deaths: no clear link to the mail or to the media.
#25: Dr. David Schwartz , age 57. Died: December 10, 2001. Murdered by stabbing with what appeared to be a sword in rural home Loudon County, Virginia. His daughter, who identifies herself as a pagan high priestess, and three of her fellow pagans have been charged. He was extremely well respected in biophysics, and regarded as an authority on DNA sequencing. Three teens that were into the occult were charged with murder in the slashing death.
#22-24:
Avishai Berkman, age 50. (no photo)
Amiramp Eldor, age 59 Yaacov Matzner, age 54
All Died: November 24, 2001
Another airplane crash kills 3 scientists. At about the time of the Black Sea crash, Israeli journalists had been sounding the alarm that two Israeli microbiologists had been murdered, allegedly by terrorists; including the head of the Hematology department at Israel’s Ichilov Hospital, as well as directors of the Tel Aviv Public Health Department and Hebrew University School of Medicine. World experts in hematology and blood clotting. Five microbiologists in this list of the first eight people that died mysteriously in airplane crashes worked on cutting edge microbiology research; and, four of the five were doing virtually identical research; research that has global political and financial significance.
#21: Jeffrey Paris Wall, age 41. Died: November 6, 2001. Body was found sprawled next to a three-story parking structure near his office. Mr. Wall had studied at the University of California, Los Angeles. He was a biomedical expert who held a medical degree, and he also specialized in patent and intellectual property.
#16-#20: Five Unnamed Microbiologists. Died: October 4, 2001. Four of Five unnamed microbiologists on a plane that was brought down by a missile near the Black sea on the Russian border. Traveling from Israel to Russia; business not disclosed. 3 scientists were experts in medical research or public health. The plane is believed by many in Israel to have had as many as four or five passengers who were microbiologists. Both Israel and Novosibirsk are homes for cutting-edge microbiological research. Novosibirsk is known as the scientific capital of Siberia. There are over 50 research facilities there, and 13 full universities for a population of only 2.5 million people.
#15: Professor Janusz Jeljaszewicz, Died: on May 7, 2001, cause not disclosed. He was an expert in Staphylococci and Staphylococcal Infections. His main scientific interests and achievements were in the mechanism of action and biological properties of staphylococcal toxins, and included the immunomodulatory properties and experimental treatment of tumors by Propionibacterium.
Died 2000
#14: Linda Reese, age 52. Died: December 25, 2000 three days after she studied a sample from Tricia Zailo, 19, a Fairfield, N.J., resident who was a sophomore at Michigan State University. Tricia Zailo died Dec. 18, a few days after she returned home for the holidays. Dr. Reese was a Microbiologist working with victims of meningitis.
#13: Mike Thomas, age 35. Died: July 16, 2000 a few days after examining a sample taken from a 12-year-old girl who was diagnosed with meningitis and survived. He was a microbiologist at the Crestwood Medical Center in Huntsville.
#12: Walter W. Shervington, M.D., age 62. Died: April 15, 2000 of cancer at Tulane Medical Hospital. He was an extensive writer/ lecturer/ researcher about mental health and AIDS in the African American community.
Died 1998
#11: Jonathan Mann, age 51. Died September 1998, in Swissair Flight 111 over Canada. He was founding director of the World Health Organization’s global Aids program and founded Project SIDA in Zaire, the most comprehensive Aids research effort in Africa at the time, and in 1986 he joined the WHO to lead the global response against Aids. He became director of WHO’s global program on Aids which later became the UNAids program. He then became director of the Francois-Xavier Bagnoud Center for Health and Human Rights, which was set up at Harvard School of Public Health in 1993. He caused controversy earlier in 1998 in the media when he accused the US National Institutes of Health of violating human rights by failing to act quickly on developing Aids vaccines.
#10: Elizabeth A. Rich, M.D., age 46. Died July 10, 1998, in a traffic accident while visiting family in Tennessee. She was an associate professor with tenure in the pulmonary division of the Department of Medicine at CWRU and University Hospitals of Cleveland. She was also a member of the executive committee for the Center for AIDS Research and directed the Bio-safety level 3 facility, a specialized laboratory for the handling of HIV, virulent TB bacteria, and other infectious agents. .
Died 1994 – 1996
#9: Sidney Harshman, age 67. Died: Dec. 25, 1997, from complications of diabetes. He was a professor of microbiology and immunology. He was the world’s leading expert on staphylococcal alpha toxins.
#6-8:
Mark Purdey, his Lawyer, and Veterinarian working with Purdey Die: CJD doctor Mark Purdey was familiar with the expression “abnormal brain protein.” Purdey’s house was burned down, his lawyer on mad cow issues was driven off the road and died and the veterinarian in the UK BSE inquiry also died in a mysterious car crash. CJD specialist Dr C. Bruton was killed in a car crash just before he went public with a new research paper. The veterinarian on the case also died in a car crash. Purdey’s new lawyer, too, had a car accident, but not fatal. Before Dr. Purdey’s death, he speculated that Dr. C. Bruton (#2 below) might have known more than what was revealed in his paper before he was killed.
#4-5
Dr. Tsunao Saitoh, age 46. Died: May 7, 1996. Shot and killed, along with his young daughter, in LaJolla, California. He was dead behind the wheel of the car, the side window had been shot out, and the door was open. His daughter appeared to have tried to run away and she was shot dead, also. The hit was compared to other killings of Japanese in this country by muggers. Expert in abnormal proteins in Alzheimer.
#3 Dr. Jawad Al Aubaidi. Died in 1994. A graduate doctor from Cornel, he was hired to head the mycoplasma biowar research project. One of Dr. Aubaidi’s projects was filling payloads of scud missles with mycoplasma strains. In 1995, Dr. Aubaidi was murdered by the Israelis Mussad. His demise, or, neutralization was made to look like an accident. He was killed in his native Iraq while he was changing a flat tire and was hit by a truck.
#2 Dr. C. Bruton, a CJD specialist — who had just produced a paper on the a new strain of CJD — was killed in a car crash before his work was announced to the public. Purdey speculates that Bruton might have known more than what was revealed in his paper.
#1 Jose Trias, Died: May 19, 1994. Trias and his wife were murdered in their Chevy Chase, Maryland home. They met with a friend of theirs, a journalist, before the day of their murder and told him of their plan to expose HHMI (Howard Hughes Medical Institute) funding of “special ops” research. Grant money that goes to HHMI is actually diverted to special black ops research projects.
http://www.whale.to/a/dead22.html
***
https://www.ancient-origins.net/news-history-archaeology/ancient-coronavirus-0015507
" Updated 27 June, 2021 - 18:26 Sahir

Ancient Coronavirus Pandemic Evidence Found in Asia
Studying the human genome gives us a fascinating glimpse into the evolution of human DNA over time. Modern technology permits scientists to discover and understand certain diseases that potentially occurred thousands of years ago, all with the help of genome evidence. A new study by an international team of researchers from the University of Adelaide and the University of Arizona of 2,500 modern humans from 26 worldwide populations revealed that an ancient coronavirus outbreak struck East Asia some 20,000 years ago!
https://content1.avplayer.com/601d9a7f2e688a79e17c1265/videos/64d35ec38b318c89a20e744d/64d35ed2c4242892a20e79f3/video.mp4
The DNA double helix molecule is the genetic blueprint for life. The recent study on the ancient coronavirus pandemic in East Asia drew on DNA and gene evidence. (nobeastsofierce / Adobe Stock)
Using Ancient Coronavirus Evidence To Fight Future Viruses
East Asia’s ancient coronavirus pandemic left traces in the genetic makeup of the people from this region, as per the open-access study published in Scientific Biology. The genes among the DNA of this population subset of East Asian ancestry, by virtue of natural selection, were better adapted to respond to the “new” (2020) coronavirus and its variants, which would have lessened the severity of the virus on these people.
A History of Nursing Heroes from Florence Nightingale to Coronavirus
What Can the Plague of Athens Teach Us About Today’s Coronavirus?
They noted that, “…modern human genomes contain evolutionary information tracing back tens of thousands of years, which may help identify the viruses that have impacted our ancestors—pointing to which viruses have future pandemic potential.”
Despite all the advanced biological and medical tools at our disposal, the current coronavirus outbreak has claimed almost 4 million lives and counting. So, more information like this from the past can help contain the impact of future viruses of this type.
Viruses are microscopic parasites, smaller than even bacteria, that are incapable of surviving on their own. They lack the capacity to live and thrive outside of a host body, and hence rely on making copies of themselves once they enter the host. Upon entering, they attach themselves to host cell surfaces, make copies, and usurp the energy of host cells by releasing their own genomes and disrupting or hijacking various parts of the cell machinery, forcing the cell to produce viral proteins.
Dr. Yassine Souilmi, from the University of Adelaide's School of Biological Sciences and the lead author on this study, agrees and adds, “Viruses are very simple creatures with the sole objective to make more copies of themselves. Their simple biological structure renders them incapable of reproducing by themselves so they must invade the cells of other organisms and hijack their molecular machinery to exist."
https://youtu.be/8_I9oVhlrjE
In the last two decades, there have been three severe coronavirus epidemics, as per Science Daily. The first was SARS-CoV, which led to Severe Acute Respiratory Syndrome which originated in China in 2002 and killed more than 800 people. The second was MERS-CoV, which led to the Middle East Respiratory Syndrome, which killed over 850 people. The third epidemic and by far the worst is the current SARS-CoV-2 (COVID-19), which has killed almost 4 million people in less than two years.

Professor Kirill Alexandrov from the CSIRO-QUT Synthetic Biology Alliance and QUT’s Centre for Genomics and Personalized Health, was part of a team of researchers from the University of Arizona, the University of California San Francisco, and the University of Adelaide who have published their findings about the ancient coronavirus “pandemic” in East Asia, in the journal Current Biology. (QUT)
The 1000 Genomes Project and Genetic Variations
The 1000 Genomes Project was launched in 2008 as a collaborative international research effort to collate, collect and establish by far the most detailed catalogue of human genetic variations.
How ‘Death Ships’ Spread Disease Through the Ages
Medieval ‘Wine Windows’ Revived Due to Coronavirus
In 2012, a detailed list was published in an open-access form in the publication Nature, which revealed a sequence of 1092 genomes. Researchers used data from this list to assess human gene coding variations and changes, to study the response and behavior of SARS-CoV-2 proteins. According to the Daily Mail, the team synthesized both human and SARS-CoV-2 proteins, showing a direct interaction that highlighted the nature of the mechanism that coronaviruses use for cell invasion.
"Computational scientists on the team applied evolutionary analysis to the human genomic dataset to discover evidence that the ancestors of East Asian people experienced an epidemic of a coronavirus-induced disease similar to COVID-19. In the course of the epidemic, selection favored variants of pathogenesis-related human genes with adaptive changes presumably leading to a less severe disease," said Professor Kirill Alexandrov from CSIRO-QUT Synthetic Biology Alliance and QUT's Centre for Genomics and Personalized Health, a co-author on the study.
The larger purpose of this project and the research it will hopefully produce is twofold. First, to collect as much data as possible, and to compile lists of a wide variety of dangerous viruses that have the potential for uncontrolled spread (unlike the current COVID-19 pandemic). Primarily, this helps in identifying “pandemic” viruses both in the distant past and in the future. This data will then be used to fund and encourage research and analysis in a bid to develop diagnostics, vaccines, and other drugs.
Secondly, old viruses, like the ancient coronavirus evidence found in the recent study, can help modern humans better understand genome sequences and DNA responses in relation to how they adapted or changed in response to past viruses.
“The modern human genome contains evolutionary information tracing back tens of thousands of years. By developing greater insights into the ancient viral foes, we gain understanding of how genomes of different human populations adapted to the viruses that have been recently recognized as a significant driver of human evolution,” concludes Professor Alexandrov.
Top image: The coronavirus up close. Evidence of an ancient coronavirus outbreak, from 20,000 years ago, has been found in the DNA of ancient East Asia populations, according to the latest study. Source: peterschreiber.media / Adobe Stock
By Rudra Bhushan "
***
Kiina ja valtion valvomat mediat
· 2. joulukuu 2020 ·
Why COVID-19 origin remains a mystery
Scientists have found new clues to where COVID-19 began. But its exact origin is still a mystery.
https://www.facebook.com/XinhuaNewsAgency/videos/847806112638069
***
Dalgleish jatkaa hölmöyksiään
https://mkrsuomi.fi/syopalaakarin-kooste-mrna-rokotteista-vihdoinkin-apua-turbosyopien-hoitoon/

SYÖPÄLÄÄKÄRIN KOOSTE MRNA-ROKOTTEISTA – VIHDOINKIN APUA ”TURBOSYÖPIEN” HOITOON
9.1.2024
ARTIKKELI JAETTAVISSA:
https://mkrsuomi.fi/syopalaakarin-kooste-mrna-rokotteista-vihdoinkin-apua-turbosyopien-hoitoon/
SYÖPÄLÄÄKÄRIN KOOSTE MRNA-ROKOTTEISTA
– VIHDOINKIN APUA ”TURBOSYÖPIEN” HOITOON
Epätavalliset ja nopeasti etenevät ns. ”Turbosyövät” ovat yleistyneet rajusti viime aikoina. Uusia syöpätapauksia ja -kuolemia ilmenee kaiken ikäisillä, niin Suomessa kuin maailmalla. Osa lääkäreistä on epäillyt syyksi vuonna 2021 aloitettua väestön altistamista kokeellisille geeniteknologisille mRNA-koronarokotuksille. Aiheesta on kertynyt paljon tieteellistä materiaalia syy-seuraus-yhteyden tueksi, mutta aihe on selvästi vielä tabu. Vaikka viranomaiset eivät halua puhua asiasta, potilaita on silti paljon ja he tarvitsevat apua välittömästi.
Ne syöpätapaukset, jotka aiheutuvat mRNA-rokotteiden monimutkaisesta geeniteknologiasta, vaativat luonnollisesti täysin uudenlaisia hoitoja parantuakseen. Kuten on nähty, perinteiset syöpähoidot eivät riitä kun aiheuttamismekanismit ovat perinteisiä syitä paljon laajemmat. Geeniteknologiasta kärsiviä syöpäpotilaita auttaaksemme ja uusia tapauksia ehkäistäksemme suomensimme kantaansa muuttaneen arvostetun syöpälääkärin, professori Angus Dalgleishin, koosteen mRNA-rokotteiden ongelmista.
Voit levittää tätä tiedeartikkelia lääkäreille, asiantuntijoille ja geeniteknologiayrityksille, jotta Suomeen syntyisi vihdoin kokonaisvaltaista ja poikkitieteellistä yhteistyötä sekä tehokkaita hoitoja näiden uuden mRNA-geeniteknologian aiheuttamien sairauksien parantamiseksi. Lähdeluettelo artikkelin lopussa.
ARTIKKELIN KIRJOITTAJASTA:
ANGUS DALGLEISH on immunologian asiantuntija ja onkologian professori St George’s Hospital Medical Schoolissa Lontoossa. Dalgleish on tutkinut laajasti syöpätauteja ja on tunnettu HIV/AIDS-tutkimustyöstään. Hän on ollut mukana kehittämässä rokotteita syöpätauteihin ja jopa rokote-ehdokasta koronaan ennen kuin näkemyksiin tuli myös kriittisyyttä mRNA-rokotteissa ilmenneisiin ongelmiin.
Prof. Angus Dalgleishilla on 495 tieteellistä julkaisua ja häntä on siteerattu 21 234 kertaa.
SUOMENNETTU KOOSTEARTIKKELI:
PROF. ANGUS DALGLEISH:
– MRNA-”ROKOTTEET” ON KIELLETTÄVÄ LOPULLISESTI
Ne meistä, jotka tiesivät alusta alkaen, että SARS-CoV-2:n sekvenssi sisälsi geenipätkiä, jotka eivät mitenkään olisi voineet syntyä luonnollisesti ja jotka olivat samankaltaisia kuin Wuhanin laboratoriosta jo julkaistut geenipätkät, ovat joutuneet kestämään uskomatonta halveksuntaa, tieteellistä hyljeksintää ja häpeällistä ”cancelointia” sekä tiedotusvälineiden että ammattikollegoiden taholta jo lähes kolmen vuoden ajan.
Kesällä 2020 sekä Yhdysvalloissa että Yhdistyneessä kuningaskunnassa tukahdutettiin julkaisu, jota olin mukana kirjoittamassa ja jossa kuvattiin englantilais-norjalaisen tutkijaryhmän tuloksia, jotka olivat osoittaneet Covid-viruksen ainutlaatuiset laboratoriossa tapahtuneen manipuloinnin ”sormenjäljet”. Tämä tapahtui samaan aikaan, kun Maailman Terveysjärjestö WHO, johtavat tiedelehdet ja muut tahot tekivät valtavasti työtä vakuuttaakseen meille, että Covid oli luonnollinen ilmiö ja että meidän pitäisi käyttää paljon enemmän rahaa tällaisten tulevien uhkien torjuntaan. (1)
Vasta nyt Telegraph-sanomalehti (2) raportoi (kritiikittömästi), että Yhdysvaltain hallitus ei enää aio rahoittaa tutkimusta, jonka tekemisen se kielsi lähes kolmen vuoden ajan ja jota tiedotusvälineet katsoivat sivusta. Silti on ollut avoin salaisuus kaikille, jotka seuraavat alkuperäislähteitä (niitä, jotka valtamedia ja erityisesti BBC jättävät huomiotta, joista Ofcom raportoi väärää tietoa ja jotka ovat Yhdistyneen kuningaskunnan hallituksen orwellilaisen Counter-Disinformation Cell -yksikön kohteena), että mRNA-rokotteet eivät tehneet sitä, mitä injektiopullossa lukee.
Ensinnäkään ”rokote” ei pysynyt injektiokohdassa, kuten luvattiin, vaan se kulkeutui koko kehoon, ja kuoleman jälkeisissä tutkimuksissa sitä todettiin olevan kaikkialla. (3)
Syytökset rokote-erien välisestä dramaattisesta vaihtelusta – mikä on ehdottomasti epätoivottava tapahtuma rokotteiden valmistusmenetelmissä – joka voisi selittää, miksi haittavaikutukset olivat yleisempiä joissakin erissä kuin toisissa, kiistettiin, mutta tanskalaiset tutkimustulokset, joista on raportoitu täällä, vahvistivat ne. https://www.conservativewoman.co.uk/vaccine-dangers-is-this-the-strongest-evidence-yet/ (4) Lääketurvallisuuden valvontaviranomaiset näyttävät sivuuttaneen nämä hälyttävät huolenaiheet, vaikka heidän olisi pitänyt välittömästi ryhtyä tutkimaan näitä perusteellisesti.
Samaan aikaan lääketurvallisuuden valvontaviranomaiset ja poliitikot ovat toistuvasti julistaneet, että (rokotehaittoihin liittyvien) Yhdistyneen kuningaskunnan Yellow Cardin ja Yhdysvaltojen VAERS-haittavaikutusraporttien lisääntyvästä huolestuttavasta määrästä huolimatta ei ole mitään syytä huoleen, toistellen kuin papukaijat vakuuttelujaan ”korkeimmista standardeista”. (5)
Viime kesäkuussa tutkijoiden Sucharit Bhakdin ja Kevin McKernanin johtamat ilmiantajat nostivat esiin aivan uuden huolenaiheen – vakavan DNA-kontaminaation. (6) Jälleen kerran valtamedia jätti tämän huomiotta. Vaikka tiedotusvälineet raportoivat mielellään rokotteiden satunnaisista sivuvaikutuksista ja korostavat, että ne ovat erittäin harvinaisia, ne eivät ole koskaan puuttuneet yhä ongelmallisempaan viralliseen ”turvallinen ja tehokas” -mantraan.
Lopulta tapahtui pieni läpimurto. Erillinen, mutta rohkeampi valtamedian edustaja Spectator Australia -lehti on vihdoin paljastanut sekä Pfizerin että Modernan mRNA Covid -rokotteiden vakavan saastumisen. (7) Artikkelissa kuvataan, kuinka bostonilainen genomitutkija Kevin McKernan käytti tutkimuksessaan Pfizerin ja Modernan injektiopulloja kontrolleina vain havaitakseen, että ne sisälsivät erittäin merkittävää DNA-plasmidikontaminaatiota. Siinä kerrotaan, että McKernan oli huolestunut havaitessaan Pfizerin rokotepulloissa SV40-promoottorin, jota ”käytetään DNA:n ohjaamiseen ytimeen erityisesti geeniterapioissa”, ja että tämä on ”jotain minkä lääketurvallisuuden valvontaviranomaiset ympäri maailmaa ovat nimenomaan kieltäneet olevan mahdollista mRNA-rokotteissa”. Nämä SV40-promoottorit ovat myös tunnetusti onkogeenisiä tai syöpää aiheuttavia.
Muut ovat vahvistaneet nämä havainnot. Saksalainen biologi on havainnut, että saastumisaste on jopa 354-kertainen suositeltuun raja-arvoon nähden. (8) Kaikesta tästä on ilmoitettu Yhdysvaltain elintarvike- ja lääkevirastolle (FDA). Se on erittäin merkittävää.
Suoraan sanottuna tämä tarkoittaa, että kyse ei ole rokotteista vaan geneettisesti muunnelluista organismeista (GMO), joihin olisi pitänyt soveltaa täysin erilaisia sääntelyehtoja eikä niitä missään nimessä olisi pitänyt luokitella rokotteiksi. Tämän on tunnustanut FDA:n australialainen versio, TGA, mikä on muuttanut kokonaiskuvaa niin paljon, että Victorian pääministeri Dan Andrews, joka oli rokotteen ja sen pakollisen käytön suurin kannattaja, on eronnut tehtävästään – vaikka tätä kirjoitettaessa rokotetta ei ole mainittu hänen eronsa syyksi. (Paula Jardine kertoi näillä sivuilla joulukuussa 2021 tästä sääntelyn kikkailusta, kun rokotteelle myönnettiin hätäkäyttöluvat, vaikka he olivat geenihoitoja.) (9)
Kaikki nämä tiedot, jotka ovat hitaasti pääsemässä julkisuuteen, tulevat kovaa vauhtia viimeisimpien havaintojen jälkeen, joiden mukaan tehosterokotteet itse asiassa lisäävät tartunnan saamisen mahdollisuutta 3,6-kertaiseksi. Tämä käy ilmi Cleveland Clinicin (yksi maailman suurimmista terveydenhuolto-organisaatioista) julkaisemasta perusteellisesta tutkimuksesta, jossa seurattiin sekä henkilökuntaa että potilaita. (10)
Tilanne pahenee. Tämän teknologian kannattajat ovat väittäneet, että sitä voidaan mukauttaa uusien varianttien jahtaamiseen. Mutta sitä ei voida. Bivalenttien rokotteiden (joissa on komponentteja vähintään kahta varianttia vastaan) tuloksissa nähdään sama tulos. Clevelandin tutkimuksen kirjoittajat sanovat, että ”ei ole yhtään tutkimusta, joka olisi osoittanut, että Covid-19-bivalenttirokote suojaa Omicron-variantin XBB-linjojen aiheuttamalta vakavalta taudilta tai kuolemalta.” Kun taas ainakin yhdessä aiemmassa tutkimuksessa ei havaittu bivalentin rokotteen suojaavaa vaikutusta SARS-CoV-2:n XBB-linjoja vastaan.
Eräässä tutkimuksessa kaikki Covidilla rokotetut hiiret sairastuivat. (11)
Monet meistä ennustivat tämän, koska SARS-virukset ovat alttiita immunologiselle leimautumiselle: kun ne ovat kerran nähneet rokotteen, ne reagoivat samalla tavalla mihin tahansa läheiseen varianttiin (tätä kutsutaan myös ”antigeeniseksi synniksi”) (12), mikä tekee uusista rokotteista paitsi hyödyttömiä, mutta myös vaarallisempia, koska ne saavat aikaan vasta-aineita, jotka vahvistavat infektiota (ADE-vasta-aineet), eivätkä saa aikaan (suojaavaa) ristireaktiota, kuten valmistajat ovat väittäneet.
mRNA-”rokotteiden” ongelmat eivät lopu tähän. Useat immunologiset tutkimukset ovat osoittaneet, että tehosterokotteet aiheuttavat vasta-aineiden vaihtumisen neutraloivista alatyypeistä ei-neutraloiviin (toleroiviin) alatyyppeihin sekä aiheuttavat merkittävää T-solujen suppressiota, mikä kaikki edistää uusia infektioita ja tukahduttaa immuunivasteen syöpää vastaan.
Viime vuoden lopulla kerroin, että melanoomapotilaat (13) , joiden tila oli ollut jo vuosia vakaa, sairastuivat uudelleen ensimmäisen tehosterokotteen (kolmannen injektion) jälkeen. Minulle sanottiin, että kyseessä oli pelkkä sattuma ja että minun oli vaiennettava asia, mutta se oli mahdotonta. Potilaideni määrä on siitä lähtien kasvanut. Näin juuri viime viikolla kaksi uutta tapausta, joissa syöpä uusiutui tehosterokotuksen jälkeen potilaillani.
Muut syöpälääkärit ovat ottaneet minuun yhteyttä kaikkialta maailmasta, myös Australiasta ja Yhdysvalloista. Yksimielisyys vallitsee siitä, että se ei enää rajoitu melanoomaan, vaan tehosterokotusten jälkeen on havaittu myös lymfoomien, leukemioiden ja munuaissyöpien lisääntynyttä esiintyvyyttä. Lisäksi kolorektaalisyöpään erikoistuneet kollegani raportoivat räjähdysmäisten syöpien epidemiasta (ne, joissa esiintyy useita etäpesäkkeitä maksassa ja muualla). Kaikki nämä syövät esiintyvät (hyvin harvoja poikkeuksia lukuun ottamatta) potilailla, joiden on ollut pakko saada Covid-rokoteboosteri, halusivatpa he sitä tai eivät, ja monet heistä ovat joutuneet matkustamaan.
Miksi näitä syöpiä siis esiintyy? T-solujen suppressio oli ensimmäinen todennäköinen selitykseni, koska immunoterapia on niin tehokasta näissä syövissä. Nyt on kuitenkin otettava huomioon myös DNA-plasmidien ja SV40:n integroituminen syövän kehittymisen edistämiseksi, ja tämä seikka on entistäkin huolestuttavampi, kun on raportoitu, että mRNA-piikkiproteiini sitoo p53:a ja muita syövän suppressorigeenejä. On hyvin selvää ja hyvin pelottavaa, että näissä rokotteissa on useita tekijöitä, jotka voivat aiheuttaa täydellisen myrskyn syövän kehittymiselle niillä potilailla, jotka ovat olleet tarpeeksi onnekkaita välttyäkseen sydänkohtauksilta, hyytymiltä, aivohalvauksilta, autoimmuunisairauksilta ja muilta Covid-rokotteiden yleisiltä haittavaikutuksilta.
Tehosterokotusten suositteleminen, kuten nyt on tapana, on vain ja ainoastaan lääketieteellistä epäpätevyyttä; sen jatkaminen edellä mainittujen tietojen perusteella on lääketieteellistä huolimattomuutta, josta voi seurata vankeusrangaistus.
Enää ei ole aikaa jossittelulle. Kaikki mRNA-rokotteet on lopetettava ja kiellettävä nyt.
ANGUS DALGLEISH
Syöpätautien professori
LISÄTIETOA KIRJOITTAJASTA:
https://en.wikipedia.org/wiki/Angus_Dalgleish
ALKUPERÄINEN ENGLANNINKIELINEN JULKAISU TIETEELLISINE LÄHDEVIITTEINEEN:
https://www.conservativewoman.co.uk/mrna-vaccines-must-be-banned-once-and-for-all/?s=09&fbclid=IwAR0-4WdcJeb47CFZ7YnX7Zj6XZEx2nHibXJzGx9rE7A0GRPL2zBDvGAkFjA
LÄHDEVIITTEET:
(1) https://www.conservativewoman.co.uk/time-to-come-clean-about-covids-lab-origins/
(2) https://www.telegraph.co.uk/world-news/2023/09/24/china-lab-wuhan-leaking-covid-loses-us-funding-experiments/
(3) https://www.conservativewoman.co.uk/major-new-autopsy-report-reveals-those-who-died-suddenly-were-likely-killed-by-the-covid-vaccine/
(4) https://www.conservativewoman.co.uk/vaccine-dangers-is-this-the-strongest-evidence-yet/
(5) https://www.conservativewoman.co.uk/shocking-report-details-mhra-failings-over-covid-vaccines/
(6) https://www.conservativewoman.co.uk/contaminated-vaccines-how-much-longer-can-the-safe-and-effective-narrative-survive/
(7) https://www.spectator.com.au/2023/09/scientists-shocked-and-alarmed-at-whats-in-the-mrna-shots/
(8) https://dailysceptic.org/2023/09/23/german-whistleblower-finds-dna-contamination-up-to-354-times-recommended-limit-in-biontech-pfizer-vaccine/
(9) https://www.conservativewoman.co.uk/uk-led-the-vaccine-rush-but-did-we-know-anything-about-gene-safety/
(10) https://dailysceptic.org/2023/06/17/new-cleveland-clinic-study-confirms-negative-efficacy-of-covid-vaccine-boosted-33-more-likely-to-get-covid/
(11) https://www.igor-chudov.com/p/all-bivalent-boosted-mice-got-covid
(12) https://en.wikipedia.org/wiki/Original_antigenic_sin
(13) https://www.conservativewoman.co.uk/other-cancer-specialists-agree-with-me-about-vaccine-harm-but-the-authorities-still-wont-listen/
LISÄTIETOJA AIHEESTA SUOMALAISILTA ASIANTUNTIJOILTA MKR YHTEISTYÖVERKOSTON KAUTTA:
www.mkrsuomi.fi "
***
Elon Musk sekoilee laboratorio-korona-salaliittoteorioihin.
Tämä ei tiedä hyvää hänen pisneksilleen Kiinassa.
Fauci on päällään virkavastuussa pandemianvoittamisessa käytettettävien tieteellisten tietojen paikkansapitävyydestä, ja "pandemian aiheuttamisesta tulisi sähkötuolia.
" Elon Musk demands charges against Anthony Fauci after NIH comes clean on funding ‘gain-of-function’ research

WASHINGTON — Elon Musk demanded the arrest and prosecution of Dr. Anthony Fauci on Friday after the National Institutes of Health came clean to Congress and admitted funding risky “gain-of-function” research in Wuhan, China, prior to the outbreak of the COVID-19 pandemic there.
“Prosecute/Fauci,” the billionaire CEO of Tesla and SpaceX and owner of social media network X tweeted, sharing The Post’s Friday front page bearing a photo of Fauci and the headline “SICK LIES.”
NIH principal deputy director Lawrence Tabak confessed Thursday at a House subcommittee hearing that the US government had indeed funded dangerous research at the Wuhan Institute of Virology, which modified bat coronaviruses shortly before the outbreak began in late 2019.
“Dr. Tabak, did NIH fund gain-of-function research at the Wuhan Institute of Virology through [Manhattan-based nonprofit] EcoHealth [Alliance]?” ”asked Rep. Debbie Lesko (R-Ariz.) of the Select Subcommittee on the Coronavirus Pandemic.
Elon Musk demanded the arrest of Dr. Anthony Fauci after the National Institutes of Health came clean to Congress about the research in Wuhan, China, about COVID-19. REUTERS
Tabak’s answer conflicts with Fauci’s several fiery denials.
“The NIH has not ever and does not now fund gain-of-function research in the Wuhan Institute of Virology,” Fauci, now 83, testified to Congress in May 2021.
Musk did not specify what criminal charges Fauci should face, though perjury and lying to Congress are obvious options and have been recommended by congressional Republicans.
Both offenses carry up to five years in prison and generally have five-year statutes of limitations.
It’s unclear if other potential charges could stem from the alleged cover-up of US funding for the Chinese labs suspected of unleashing the lethal respiratory virus, which has killed at least 1,190,546 US residents, according to Centers for Disease Control and Prevention data, in addition to causing enormous economic, social and educational damage across the world.
Fauci served as President Biden’s chief medical adviser in 2021 and 2022 after presenting himself in the early phase of the pandemic as a beacon of reason and good health guidance, though allies of former President Donald Trump noted his often inconsistent tips, including on mask-wearing.
The doctor also led NIH’s National Institute of Allergy and Infectious Diseases from 1984 through the end of 2022.
Documents published in late 2021 by the Intercept revealed that the EcoHealth Alliance used grants from Fauci’s agency to fund Wuhan Institute of Virology experiments that modified three bat coronaviruses distinct from COVID-19.
The research discovered the viruses became much more infectious among “humanized” mice when human-type receptors were added to them.
(Hewompaskaa)
The Department of Health and Human Services, which includes NIH, on Tuesday barred EcoHealth from receiving federal funding for the next three years.
Tabak’s answer conflicts with Fauci’s several fiery denials, according to reports. Getty Images
The origins of COVID-19 remain a mystery due to the Chinese government’s refusal to allow an independent international investigation.
Musk did not specify what criminal charges Fauci should face, though perjury and lying to Congress are obvious options and have been recommended by congressional Republicans. REUTERS
Some parts of the US government, including the FBI and the Energy Department — which includes the US National Laboratories — believe the pandemic emerged via a lab leak in China.
Biden has said very little about determining the origins of the pandemic. Trump, his predecessor and November election challenger, has proposed forcing China to pay $10 trillion in “reparations.”
Trimp ei puhu mitään mistään "virusten modifioinneista".
"Tupakki-Lawrece" on hammaslääkäri ja kasvoluuortopedi.
***
https://www.facebook.com/BenSwannRealityCheck/videos/138802464973099
" Fauci Lies Again, Pretends He Doesn't Know What Went On In Wuhan Lab
Media is now claiming "NEW" information that indicates that Covid came from the Wuhan Lab. But for those of us who have been following this story, this is not new information... this evidence has been known for over a year. So why is Dr. Fauci, now suddenly pretending that he believe Covid could have come from a lab? "
***
https://www.facebook.com/XinhuaNewsAgency/videos/148560010689142
oli live-tilassa.
LIVE: China holds news briefing on origin-tracing of COVID-19
LIVE: China's State Council Information Office holds a news conference on origin-tracing of #COVID19.
***
PDF
Tiivistelmä
COVID-19-pandemian oppien yhteenveto:
-
Pandemian alkuperä:
- SARS-CoV-2-viruksen alkuperäksi esitetään enenevässä määrin laboratoriolähtöistä onnettomuutta Wuhanin virologian instituutissa (WIV). Useat tiedusteluviranomaiset ja asiantuntijat tukevat tätä teoriaa.
- Raportti viittaa siihen, että Wuhanin instituutti harjoitti "gain-of-function" -tutkimusta, jolla pyrittiin muuttamaan virusten ominaisuuksia.
- Erityisesti Anthony Faucin ja muiden tutkijoiden toimia tarkasteltiin pandemian alkuperää koskevien teorioiden ympärillä.
-
Yhdysvaltain vastaus:
- Operaatio Warp Speed -rokotehanke oli suuri menestys, mutta hallituksen pandemiavastetta varjostivat laajamittainen petos, resurssien väärinkäyttö ja tehottomuus.
- Pandemia-aikana toteutetut koulujen sulkemiset ja muut rajoitustoimet arvioitiin vahingollisiksi erityisesti lasten oppimisen, mielenterveyden ja fyysisen hyvinvoinnin osalta.
-
Andrew Cuomon hallinnon toimet:
- Raportti syyttää entistä New Yorkin kuvernööriä Andrew Cuomoa lääketieteellisestä virheestä sekä hoitokodeissa tapahtuneiden kuolemien peittelystä.
-
WHO ja kansainvälinen yhteistyö:
- Maailman terveysjärjestön (WHO) rooli pandemian hallinnassa arvioitiin puutteelliseksi, erityisesti Kiinan vaikutusvallan vuoksi.
-
Maskit ja sosiaalinen etäisyys:
- Maskien ja sosiaalisen etäisyyden hyödyllisyydestä esitettiin ristiriitaisia näkemyksiä. Raportti korostaa tutkimusten puutteellisuutta ja julkisen viestinnän epäselvyyksiä.
-
Taloudellinen vaikutus:
- Pandemian aiheuttamat taloudelliset toimenpiteet, kuten Paycheck Protection Program (PPP), kärsivät laajasta petoksesta ja heikosta valvonnasta, mikä johti miljardien dollarien väärinkäytöksiin.
-
Lääke- ja rokotepolitiikka:
- Rokotepakot ja niiden tieteellinen perusta kyseenalaistettiin. Raportti painottaa luonnollisen immuniteetin merkitystä ja tuo esille rokotteiden turvallisuuteen liittyviä kysymyksiä.
Johtopäätökset: Raportti painottaa läpinäkyvyyden, vastuullisuuden ja yhteistyön merkitystä tulevien pandemioiden hallinnassa. Sen mukaan Yhdysvaltojen on varauduttava paremmin vähentämällä riippuvuutta ulkomaisista lääketieteellisistä tarvikkeista ja uudistamalla terveydenhuollon valmiusjärjestelmiä.
Tarvitsetko tarkempia osioita tai tiettyjen henkilöiden toimien analysointia?
Pandemian alkuperä (Raportin avaus)
1. SARS-CoV-2:n alkuperä:
- Raportti korostaa kasvavaa todistusaineistoa, jonka mukaan SARS-CoV-2-virus sai alkunsa laboratoriotai tutkimusperäisestä onnettomuudesta Wuhanin virologian instituutissa (WIV).
- Keskeiset havainnot:
- Yhdysvaltain ulkoministeriön vuonna 2021 julkaisema raportti totesi, että useat WIV:n tutkijat sairastuivat syksyllä 2019 oirein, jotka viittasivat sekä COVID-19:ään että kausi-influenssaan.
- Instituutti oli harjoittanut gain-of-function-tutkimusta, jossa yhdistettiin SARS-kaltaisia koronaviruksia ja käytettiin geenimuokkauksia luomaan uusia viruksia. Osa tästä työstä suoritettiin vajailla turvallisuusmääräyksillä (BSL-2-taso).
- Wuhanin virologian instituutti oli tehnyt yhteistyötä Kiinan armeijan kanssa vuodesta 2017 lähtien, mikä lisäsi epäilyjä mahdollisista sotilaallisista tutkimustarkoituksista.
2. Labra-onnettomuuden puolesta puhuva todistusaineisto:
- Useat korkea-arvoiset tiedusteluviranomaiset, tiedemiehet ja toimittajat, kuten John Ratcliffe ja Dr. Robert Redfield, tukevat teoriaa.
- Dr. Redfield (entinen CDC:n johtaja) totesi maaliskuussa 2023, että COVID-19:n nopea leviämiskyky ihmisestä toiseen viittaa viruksen syntyyn laboratoriossa, eikä luonnolliseen spillover-tapahtumaan.
- Nicholas Wade korosti furin-halkaisupaikan (ominaisuus, joka mahdollisti viruksen helpon leviämisen ihmisiin) olevan ainutlaatuinen SARS-CoV-2:lle ja sopivan yhteen WIV:n suunnitteleman tutkimuksen kanssa.
3. Vaihtoehtoinen zoonoosi-teoria:
- Raportti käy läpi luonnolliseen alkuperään viittaavia tutkimuksia, mutta toteaa niiden olevan puutteellisia. Keskeisiä ongelmia:
- Wuhanin eläintoreilta tai niiden toimitusketjuista ei löydetty tartunnan saaneita eläimiä.
- Luonnollisille spillover-tapauksille tyypillisiä todisteita, kuten eläimistä löytyneitä viruksen esiasteita, ei ole löydetty (toisin kuin aiemmissa SARS- ja MERS-epidemioissa).
4. Tieteellinen painostus ja peittely:
- Raportti syyttää useita henkilöitä, kuten Dr. Anthony Faucia, siitä, että he painostivat tutkijoita tukemaan zoonoosi-teoriaa. Esimerkiksi helmikuussa 2020 julkaistu "The Proximal Origin of SARS-CoV-2" -artikkeli oli Faucin ja Dr. Francis Collinsin "ohjaama", tarkoituksena heikentää labra-teorian uskottavuutta.
5. Johtopäätökset:
- Raportti painottaa, että pandemian alkuperän selvittäminen on kriittistä tulevien pandemioiden ehkäisemiseksi.
- Se esittää todisteita, jotka vahvistavat laboratorioteoriaa ja korostavat Kiinan hallinnon sekä kansainvälisten tutkijoiden pyrkimyksiä peitellä viruksen alkuperään liittyviä tietoja.
Tarvitsetko yksityiskohtaisempia tietoja tämän kohdan eri näkökulmista, kuten yksittäisistä henkilöistä tai tutkimusprojekteista?
Sinä sanoit:
Edetään kohtaan 2. Yhdysvaltain vastaus. Kerro Warp Speed -rokotehankkeesta ja sulku-/rajoitustoimien haitallisuudesta. Onko raportissa mitään viittauksia siihen, kuinka useampi eri firma sai rokotteensa lähes samanaikaisesti markkinoille? Oliko virus Yhdysvaltain tilaama (virallisesti tai epäsuorasti)?
ChatGPT sanoi:
Oikolue tämä raportti ja tuota siitä suomenkielinen tiivistelmä. Ole tarkkana säilyttääksesi kaikki henkilöiden nimet, joihin raportissa viitataan. Jos referointi on liian iso, niin tehdään se osissa.
" Raportti on erittäin laaja ja sisältää yksityiskohtaisia havaintoja koronaviruspandemian alkuperästä, Yhdysvaltojen vastauksesta sekä useiden henkilöiden ja instituutioiden toiminnasta. Tiivistetään alkuun raportin pääkohdat, ja jos yksityiskohtaisempi analyysi tarvitaan, voimme tarkastella osia erikseen.
2. Yhdysvaltain vastaus COVID-19-pandemiaan
Raportti käsittelee laajasti Yhdysvaltain hallituksen vastatoimia COVID-19-pandemian aikana, keskittyen erityisesti Operaatio Warp Speed -rokotehankkeen onnistumisiin ja sulku- ja rajoitustoimien haitallisiin seurauksiin. Se sisältää myös pohdintaa viruksen alkuperän mahdollisesta yhteydestä Yhdysvaltain tutkimusrahoitukseen, mutta ei tue väitettä, että Yhdysvallat olisi "tilannut" virusta.
Operaatio Warp Speed -rokotehanke
-
Tavoitteet ja saavutukset:
- Operaatio Warp Speed (OWS) oli liittovaltion ja yksityisen sektorin yhteistyöhanke, jonka tavoitteena oli nopeuttaa COVID-19-rokotteiden kehitystä ja jakelua.
- Raportin mukaan hanke oli "huikea menestys", joka auttoi kehittämään ja levittämään rokotteita historiallisen nopeasti.
- Raportissa mainitaan, että hanke pelasti miljoonia ihmishenkiä vähentämällä vakavia tautitapauksia ja kuolemia.
-
Useiden rokotteiden yhtäaikainen kehitys:
- Raportti korostaa, että Warp Speedin merkittävä saavutus oli kyky mahdollistaa useiden eri valmistajien (Pfizer, Moderna, Johnson & Johnson) tuoda rokotteensa markkinoille lähes samanaikaisesti.
- Tämä onnistui hajauttamalla riskit ja rahoittamalla useita rinnakkaisia tutkimuksia.
- mRNA-rokotteiden kehitys mainitaan erityisesti teknologisena läpimurtona.
-
Yksityisen ja julkisen sektorin yhteistyö:
- Raportti kiittää yksityisen sektorin roolia, erityisesti lääkeyhtiöitä ja logistiikkayrityksiä, joiden yhteistyö hallituksen kanssa mahdollisti nopean tuotannon ja jakelun.
- Huomautuksena todetaan kuitenkin, että hallinnolliset viivästykset ja byrokratia olisivat voineet vaarantaa onnistumisen ilman hätäratkaisuja.
-
Rokotteisiin liittyvä epäluottamus:
- Raportti mainitsee, että alkuvaiheen epäluottamus, johon vaikuttivat myös poliittiset kannanotot, hidasti rokotuskampanjan etenemistä. Esimerkiksi silloinen varapresidenttiehdokas Kamala Harris kritisoi Warp Speedin luotettavuutta, mikä vaikutti yleiseen mielipiteeseen.
Sulku- ja rajoitustoimet
-
Koulujen sulkemiset:
- Koulujen pitkät sulut arvioitiin tieteellisesti perusteettomiksi ja niiden haitallisia vaikutuksia pidettiin laaja-alaisina.
- Sulkemiset heikensivät oppimistuloksia ja lisäsivät lasten ja nuorten mielenterveysongelmia.
-
Taloudelliset vaikutukset:
- Pakolliset sulut ja laajat lockdown-toimet aiheuttivat merkittäviä taloudellisia menetyksiä.
- Raportti korostaa, että pienyritykset kärsivät suhteettoman paljon, erityisesti maaseutu- ja vähävaraisilla alueilla.
-
Rajoitustoimien haitat:
- Raportti nostaa esille, että rajoitukset heikensivät mielenterveyttä, lisäsivät päihteiden käyttöä ja pahensivat kroonisia sairauksia, koska ihmiset eivät hakeutuneet hoitoon ajoissa.
- Yksityisyyden loukkaamisen ja liikkumisvapauden rajoittamisen todettiin myös heikentäneen luottamusta julkiseen terveydenhuoltoon.
-
"Lääke pahempi kuin tauti":
- Raportti painottaa, että pandemian aikana tehdyt päätökset eivät saisi aiheuttaa enemmän haittaa kuin itse sairaus. Ylikireät lockdownit mainitaan tässä yhteydessä erityisen ongelmallisina.
Onko virus "tilattu" Yhdysvaltain toimesta?
-
Raportissa viitataan Yhdysvaltain rahoittamaan gain-of-function-tutkimukseen Wuhanin virologian instituutissa (WIV).
- EcoHealth Alliance -järjestön kautta kanavoidut varat käytettiin hankkeisiin, joissa manipuloitiin SARS-kaltaisia koronaviruksia.
- Yhdysvaltain National Institutes of Health (NIH) ja sen alainen NIAID (jota johti Dr. Anthony Fauci) eivät valvoneet EcoHealthin hankkeita riittävästi.
-
Raportti ei väitä, että virus olisi "tilattu" Yhdysvaltain toimesta. Se kuitenkin kritisoi NIH:n ja EcoHealthin yhteistyötä Kiinan kanssa ilman riittävää avoimuutta tai valvontaa.
Johtopäätökset:
- Operaatio Warp Speed oli poikkeuksellinen menestys, mutta rajoitustoimien aiheuttamat vahingot korostavat tarvetta harkituille ja tasapainoisille päätöksille pandemioiden aikana.
- Rahoituksen ja vastuunjaon puutteet tutkimushankkeissa, erityisesti EcoHealthin ja WIV:n yhteistyössä, lisäävät spekulaatioita pandemian alkuperästä.
Haluatko syventää EcoHealth Alliancen roolia tai lockdownien vaikutuksia?
Sinä sanoit:
Kyllä, kerro lisää EcoHealth Alliancesta ja sen takana operoivista henkilöistä/tahoista. Mainitaanko siinä gain-of-function tutkimuksen rahoittaminen tavoitteena luoda tehoklaampia viruksia?
EcoHealth Alliance ja sen rooli COVID-19-pandemian alkuperässä
Raportti käsittelee laajasti EcoHealth Alliance -järjestön toimintaa, joka oli keskeinen toimija gain-of-function (GOF) -tutkimuksen rahoittamisessa ja toteuttamisessa. Tämä tutkimus sisälsi vaarallisia kokeita, joissa SARS-kaltaisia koronaviruksia muokattiin geneettisesti niiden ominaisuuksien parantamiseksi. Tällainen tutkimus mahdollisti virusten tarttuvuuden ja leviämisen tehokkuuden kasvattamisen – piirteen, jota pidetään COVID-19-viruksen keskeisenä piirteenä.
EcoHealth Alliance ja sen toiminta
-
Organisaation tehtävä:
- EcoHealth Alliance on yhdysvaltalainen kansalaisjärjestö, joka keskittyy zoonoosivirusten tutkimukseen ja niiden leviämisen estämiseen.
- Sitä johti Dr. Peter Daszak, joka toimi myös keskeisenä tiedottajana pandemian alkuvaiheessa ja puolusti zoonoositeoriaa viruksen alkuperänä.
-
Rahoitus ja yhteistyö:
- EcoHealth Alliance sai merkittävää rahoitusta Yhdysvaltain National Institutes of Health (NIH) -organisaatiolta ja erityisesti sen alaiselta National Institute of Allergy and Infectious Diseases (NIAID) -instituutilta, jota johti Dr. Anthony Fauci.
- Nämä varat ohjattiin Wuhanin virologian instituutille (WIV) tutkimusprojekteihin, jotka sisälsivät SARS-kaltaisten virusten geneettistä muokkausta.
Gain-of-function (GOF) -tutkimus ja sen tavoitteet
-
Tutkimuksen luonne:
- GOF-tutkimuksen tarkoituksena oli parantaa virusten ominaisuuksia:
- Tarttuvuus: Kyky siirtyä tehokkaammin isännästä toiseen.
- Patogeenisuus: Viruksen kyky aiheuttaa vakavampaa tautia.
- Tämä toteutettiin esimerkiksi liittämällä viruksiin furin-halkaisupaikkoja, mikä lisäsi niiden kykyä tarttua ihmisen soluihin – piirre, joka löytyy SARS-CoV-2-viruksesta.
-
Rahoituksen ongelmat:
- Raportti syyttää EcoHealth Alliancea ja NIH:ta huonosta valvonnasta ja tiedottamisesta.
- EcoHealth jätti raportoimatta vaaralliset kokeet ajoissa NIH:lle, mukaan lukien kokeet, joissa syntetisoitiin SARS-kaltaisia viruksia, jotka olivat tarttuvampia kuin alkuperäiset.
- Vuoden 2018 DEFUSE-hanke: EcoHealth haki Yhdysvaltain puolustusministeriön alaiselta DARPA:lta rahoitusta luodakseen SARS-kaltaisen viruksen, jossa oli furin-halkaisupaikka. Hakemus hylättiin sen sisältämän GOF-tutkimuksen riskien vuoksi.
Keskeiset henkilöt ja tahot
-
Dr. Peter Daszak (EcoHealth Alliance):
- Johti järjestöä ja puolusti vahvasti zoonoositeoriaa pandemian alkuperästä.
- Raportin mukaan Daszak tahallisesti vääristeli tietoa tutkimusraporteissa ja julkisessa tiedottamisessa. Hän myös toimi yhteyshenkilönä WIV:n ja Yhdysvaltain rahoittajien välillä.
-
Dr. Anthony Fauci (NIAID):
- Valvoi NIH:n rahoitusta ja puolusti zoonoositeoriaa pandemian alkuvaiheessa.
- Raportti viittaa siihen, että Fauci ja hänen kollegansa vaikuttivat aktiivisesti pandemian alkuperästä käytyyn keskusteluun ja pyrkivät heikentämään labra-teorian uskottavuutta.
-
Wuhanin virologian instituutti (WIV):
- Kiinan johtava SARS-virusten tutkimuskeskus, joka oli keskeinen yhteistyökumppani EcoHealthin projekteissa.
- Raportti väittää, että WIV:ssä tehty tutkimus sisälsi puutteellisia turvallisuusprotokollia (BSL-2-taso), jotka lisäsivät onnettomuuden riskiä.
Raportin johtopäätökset GOF-tutkimuksesta
-
Yhdysvaltain rahoitus ja vastuu:
- Vaikka raportti ei suoraan väitä, että Yhdysvallat "tilasi" SARS-CoV-2-viruksen, se painottaa, että rahoitus mahdollisti riskialttiiden tutkimusten suorittamisen, jotka saattoivat johtaa pandemian syttymiseen.
- NIH ja EcoHealth eivät noudattaneet riittävää valvontaa rahoitetuissa projekteissa.
-
Tavoite tehokkaampien virusten luomisesta:
- Raportti esittää, että EcoHealthin ja WIV:n tutkimusten tavoitteena oli tutkia ja mahdollisesti luoda tehokkaampia viruksia osana pandemioiden ennaltaehkäisyä. Tämä lisää merkittävästi spekulaatioita siitä, että SARS-CoV-2 voisi olla laboratorio-onnettomuuden tulos.
Haluatko tarkempia tietoja GOF-tutkimukseen liittyvistä kokeista, henkilötodistuksista tai rahoituksen yksityiskohdista?
Sinä sanoit:
Minkälaisia toimia Andrew Cuomo teki ja miten ne liittyvät tähän kokonaisuuteen? Onko raportissa mainittu nukutusaine Midazolam tai muita lääkeinteraktioita, jotka aiheuttivat pandemian alkuvaiheissa tukehtumiskuolemia, joiden perusteella "flatten the curve" -propagandaa vahvistettiin?
WHO:n osuus COVID-19-pandemian aikana
Raportissa käsitellään Maailman terveysjärjestön (WHO) roolia COVID-19-pandemian hallinnassa ja kritisoidaan voimakkaasti sen toimintaa. WHO:n toimintaa pidetään puutteellisena, ja raportti väittää, että järjestö oli altis Kiina-keskeiselle painostukselle ja osallistui hätätilapaniikin lietsomiseen.
Keskeiset havainnot WHO:n roolista
-
Kiina-keskeisyys ja läpinäkyvyyden puute:
- WHO:n kerrotaan toimineen Kiinan kommunistisen puolueen (CCP) vaikutuksen alaisena pandemian alkuvaiheessa.
- WHO aliarvioi tai jätti huomiotta todisteet, jotka viittasivat siihen, että Kiina viivytteli tiedottamista viruksen leviämisestä ja sen vaarallisuudesta.
- WHO kieltäytyi kutsumasta virologeja, jotka olisivat voineet selvittää pandemian alkuperää riippumattomasti.
-
Kiistanalainen pandemian julistus:
- Raportti ei nimenomaisesti mainitse, että WHO olisi muuttanut pandemian määritelmää juuri ennen COVID-19:n julistamista maailmanlaajuiseksi hätätilaksi.
- Se kuitenkin viittaa siihen, että WHO toimi liian nopeasti ja ilman riittävää tieteellistä perustaa julistaessaan COVID-19-pandemian kansainväliseksi kansanterveydelliseksi hätätilanteeksi (Public Health Emergency of International Concern, PHEIC).
-
Kiinan tiedonvälityksen hyväksyntä:
- WHO hyväksyi Kiinalta saadut raportit siitä, ettei virus ollut helposti tarttuva ihmiseltä toiselle, vaikka muut maat esittivät päinvastaisia todisteita.
- Tämä johti viivästyneisiin toimiin maailmanlaajuisesti ja pahensi pandemian leviämistä.
-
Kiistanalaiset ohjeet:
- WHO:n maskien, sosiaalisen etäisyyden ja matkustusrajoitusten suosituksia kritisoidaan raportissa. Ohjeet muuttuivat usein, mikä heikensi luottamusta järjestöön.
- Erityisesti WHO:n alkuperäinen kieltäytyminen suosittelemasta maskien käyttöä ja myöhemmin muuttunut kanta nostettiin esiin.
-
Pandemiasopimus ja sen vaarat:
- WHO:n ehdottama pandemiasopimus (Pandemic Treaty) arvioitiin raportissa haitalliseksi Yhdysvalloille.
- Sopimus saattaisi lisätä WHO:n valtaa pandemiatilanteissa ilman, että järjestön perusongelmia, kuten riippuvuutta Kiinan vaikutuksesta, olisi ratkaistu.
Pandemian määritelmän muutos
- Pandemian määritelmän muutoksesta:
- Raportissa ei suoraan mainita WHO:n muuttaneen pandemian määritelmää juuri ennen COVID-19:n julistamista pandemiaksi.
- Aiemmin on kuitenkin raportoitu, että WHO yksinkertaisti pandemian määritelmää poistamalla kriteerit kuolleisuuden ja vakavuuden osalta, mikä olisi mahdollistanut lievemmän taudin, kuten COVID-19:n, luokittelun pandemiaksi.
WHO:n toimien vaikutus paniikkiin
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Hätätilapaniikin lietsominen:
- Raportti viittaa siihen, että WHO:n hätätilajulistukset ja ristiriitaiset suositukset johtivat globaalin paniikin syntymiseen, mikä pahensi taloudellisia ja sosiaalisia vaikutuksia.
- Erityisesti WHO:n alkuvaiheen epämääräiset lausunnot ja myöhemmin muuttuneet linjaukset lisäsivät yleisön epävarmuutta.
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WHO:n riippuvuus jäsenvaltioista:
- Raportti huomauttaa, että WHO on taloudellisesti riippuvainen jäsenvaltioiden ja yksityisten toimijoiden rahoituksesta, mikä tekee siitä alttiin poliittiselle vaikutukselle.
Johtopäätökset WHO:n roolista
- Raportti kehottaa uudistamaan WHO:n toimintaa, jotta se voisi toimia riippumattomasti ja tehokkaasti tulevissa pandemioissa.
- WHO:n katsotaan epäonnistuneen tehtävässään pandemian hallinnassa, erityisesti alkuvaiheessa, ja sen toimien kerrotaan pahentaneen globaalin pandemiapaniikin vaikutuksia.
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- Published: 14 May 2021
Author Correction: Molecular interaction and inhibition of SARS-CoV-2 binding to the ACE2 receptor
Nature Communications volume 12, Article number: 2996 (2021) Cite this article
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Abstract
Study of the interactions established between the viral glycoproteins and their host receptors is of critical importance for a better understanding of virus entry into cells. The novel coronavirus SARS-CoV-2 entry into host cells is mediated by its spike glycoprotein (S-glycoprotein), and the angiotensin-converting enzyme 2 (ACE2) has been identified as a cellular receptor. Here, we use atomic force microscopy to investigate the mechanisms by which the S-glycoprotein binds to the ACE2 receptor. We demonstrate, both on model surfaces and on living cells, that the receptor binding domain (RBD) serves as the binding interface within the S-glycoprotein with the ACE2 receptor and extract the kinetic and thermodynamic properties of this binding pocket. Altogether, these results provide a picture of the established interaction on living cells. Finally, we test several binding inhibitor peptides targeting the virus early attachment stages, offering new perspectives in the treatment of the SARS-CoV-2 infection.
Introduction
In December 2019, a novel coronavirus (CoV) was determined to be responsible for an outbreak of potentially fatal atypical pneumonia, ultimately defined as coronavirus disease-19 (COVID-19), in Wuhan, China. This novel CoV, termed severe acute respiratory syndrome (SARS)-CoV-2, was found to share similarities with the SARS-CoV that was responsible for the SARS pandemic that occurred in 2002. The resulting outbreak of COVID-19 has emerged as a severe pandemic. The genome of SARS-CoV-2 shares about 80% identity with that of SARS-CoV and is about 96% identical to the bat coronavirus BatCoV RaTG13 (ref. 1).
CoV entry into host cells is mediated by its transmembrane spike (S) glycoprotein that forms homotrimers protruding from the viral surface2 (Fig. 1a). The S glycoprotein comprises two functional subunits responsible either for binding to the host cell receptor (S1 subunit including the receptor-binding domain (RBD)) or for fusion of the viral and cellular membranes (S2 subunit). Recent studies claimed that the angiotensin-converting enzyme 2 (ACE2), previously identified as the cellular receptor for SARS-CoV, also acts as a receptor of the new coronavirus (SARS-CoV-2)3 (Fig. 1b). In the case of SARS-CoV, the S glycoprotein on the virion surface mediates receptor recognition (Fig. 1c) and membrane fusion4,5. Recently, the high-resolution cryo-electron microscopy structure obtained on the full-length human ACE2 in the presence of the RBD of the S glycoprotein of SARS-CoV-2 suggests simultaneous binding of two S-glycoprotein trimers to an ACE2 dimer3. The S2 subunit is further cleaved by host proteases located immediately upstream of the fusion peptide6, leading to the activation of the glycoprotein that undergoes extensive irreversible conformational changes facilitating the membrane fusion process. Altogether, the information obtained so far highlights the fact that CoV entry into susceptible cells is a complex process that requires the concerted action of receptor binding and proteolytic activation of the S glycoprotein at the host cell surface to finally promote virus – cell membrane fusion. However, so far, direct evidence about the dynamics of the binding of the S1- to the ACE2 receptor at the single-molecule level is missing.
Fig. 1: Probing SARS-CoV-2 binding to the ACE2 host receptor.

a Schematic of a SARS-CoV-2 particle, an enveloped ssRNA virus expressing at its surface the spike glycoprotein (S) that mediates the binding to host cells.
b Structural studies have previously obtained a complex between the receptor-binding domain (RBD, a subunit of the S glycoprotein) and the angiotensin-converting enzyme 2 (ACE2) receptor.
c Schematic of probing SARS-CoV-2 binding using atomic force microscopy (AFM). The initial attachment of SARS-CoV-2 to cells involves specific binding between the viral S glycoprotein and the cellular receptor, ACE2. The interactions are monitored by AFM on model surfaces, where the ACE2 receptor is attached to a surface and the S1 subunit or the RBD onto the AFM tip, and on A549 living cells expressing or not fluorescently labeled ACE2.
Here, we analyze the biophysical properties of the SARS-CoV-2 S-glycoprotein binding, on model surfaces and on living cells, to ACE2 receptors using force–distance (FD) curve-based atomic force microscopy (FD-curve-based AFM) (Fig. 1c). We extract the kinetics and thermodynamics of the interactions established in vitro, and compare the binding properties of both the S1 subunit and RBD. Next, we test short ACE2-derived peptides targeting the viral S glycoprotein as potent binding inhibitor peptides and observe a significant reduction in the binding properties.
Results
S1 subunit specifically binds to purified ACE2 receptors
As SARS-CoV-2 binding to ACE2 receptors is thought to play a key role in the first binding step at the cellular membrane3, we first used FD-curve-based AFM to evaluate at the single-molecule level the binding strength of the interaction established between the glycosylated S1 subunit and ACE2 receptors on model surfaces (Fig. 2a). To mimic cell-surface receptors in vitro, ACE2 receptors were covalently immobilized onto gold surfaces coated with OH- and COOH-terminated alkanethiols using carbodiimide conjugation (see Methods). These model surfaces were imaged by AFM, and the thickness of the grafted layer was validated by a scratching experiment, revealing a deposited layer of 6.1 ± 0.4 nm (mean ± S.D., N = 3) (see Methods and Supplementary Fig. 1). To study the interaction between the S1 subunit and the immobilized ACE2 receptors, we covalently grafted either the purified full S1 subunit or RBD only to the free end of a long polyethylene glycol (PEG)24 spacer attached to the AFM tip7,8,9. To investigate the properties of the binding complex, force–distance (FD) curves were recorded by repeatedly approaching and withdrawing the S1 subunit or RBD- functionalized tip from the ACE2 model surface (Fig. 2a, b). Specific adhesion events were observed on 4–5% of the retraction FD curves at rupture distances >15 nm, which corresponds to the extension of the PEG linker (Fig. 2c and Supplementary Fig. 2), and is in line with studies carried out for other virus–cell-surface receptor systems8,10,11,12. To confirm the specificity of these interactions, we conducted additional independent control experiments using (i) an AFM tip only functionalized with the PEG linker or (ii) toward OH-/COOH-terminated alkanethiol surfaces missing the receptor. The binding frequency observed during those control experiments is significantly lower, thereby confirming the specificity of the S1 subunit/RBD–ACE2 complexes under our experimental conditions (Fig. 2c).
Fig. 2: Probing S-glycoprotein binding to the ACE2 host receptor on model surface.

a Binding of S-glycoprotein subunit (S1 or RBD) is probed on an ACE2-coated surface.
b Retraction part of four force–distance curves showing either nonadhesive or specific adhesive curves.
c Box plot of specific binding probabilities (BP) measured by AFM between the functionalized tip (S1, RBD, or PEG) and the grafted surface (ACE2 or OH-/COOH-terminated alkanethiol (bare surface)). One data point belongs to the BP from one map acquired at 1 µm/s retraction speed. The square in the box indicates mean, the colored box indicates the 25th and 75th percentiles, and the whiskers indicate the highest and the lowest values of the results. The line in the box indicates median. N = 12 (S1, RBD), 18 (PEG), and 9 (S1, RBD vs. bare surface) maps examined over 4 (S1, RBD), 6 (PEG), and 3 (S1, RBD vs. bare surface) independent experiments.
d Bell–Evans model describing a virus-receptor bond as a two-state model. The bound state is separated from the unbound state by a single energy barrier located at distance xu. koff and kon represent the dissociation and association rate, respectively.
e, f Dynamic force spectroscopy (DFS) plot showing the distribution of the rupture forces as a function of their loading rate (LR) measured either between the S1 subunit and the ACE2 receptor (N = 1052 data points) (e) or between the RBD and the ACE2 receptor (N = 1490 data points) (f). The error bar indicates s.d. of the mean value for a single interaction (0–200 pN). The solid line represents the fit of the data with the Bell–Evans fit. Experiments were reproduced at least four times with independent tips and samples.
g, h The BP is plotted as a function of the contact time for S1 subunit and RBD on ACE2 model surfaces, and data points were fitted using a least-squares fit of a monoexponential growth. One data point belongs to the BP from one map acquired at 1 µm/s retraction speed for the different contact times. Experiments were reproduced three times with independent tips and samples. P values were determined by two-sample t test in Origin. The error bar indicates s.d. of the mean value. Source data are provided as a Source Data file.
Exploring the dynamics of S1 subunit–ACE2 interaction
Single-molecule force-probing techniques, such as FD-based AFM, measure the strength of a bond under an externally applied force, enabling to get insights into the binding free-energy landscape. According to the Bell–Evans model13,14, an external force stressing a bond reduces the activation-energy barrier toward dissociation and, hence, reduces the lifetime of the ligand-receptor pair15 (Fig. 2d). The model also predicts that far-from-equilibrium, the binding strength of the ligand-receptor bond is proportional to the logarithm of the loading rate (LR), which describes the force applied on the bond over time. To investigate the kinetics of the probed complex, FD curves were recorded at various retraction rates and contact times (Fig. 2e–h). Dynamic force spectroscopy (DFS) plots were obtained for both S1 subunit (Fig. 2e) and RBD (Fig. 2f) binding toward immobilized ACE2 receptors. In each case, the unbinding force increases linearly with the logarithm of the LR, as observed earlier for other virus-receptor bonds8,10,11,16,17. To determine whether single- or multiple-bond rupture between S1/RBD and ACE2 is taking place, bond strengths (every single gray data point in Fig. 2e, f) were analyzed through distinct discrete ranges of LRs, plotted as force histograms and further fitted with multipeak Gaussian distribution, as established previously11,16 (Supplementary Figs. 3 and 4). Using this distribution, we are able to determine the most probable unbinding force of each force peak (maximum of rupture force distribution; black dots plotted over mean LR of this range in Fig. 2e, f), and can determine if single or multiple interactions were taking place. The presence of multiple parallel unbinding events is first observed in the distribution of rupture forces with the presence of multiple Gaussian fits. The histograms show that most probably only single interactions were taking place; thus, the Bell–Evans model15 was used to fit the data enabling to interpret the binding complex as a simple two-state model, in which the bound state is separated from the unbound state by a single energy barrier (Fig. 2d). From the slope of the fit, we estimated the length scale of the energy barrier (xu). We obtained very close values, xu = 0.81 ± 0.05 nm and 0.79 ± 0.04 nm for both the S1 subunit and RBD, showing that we are probing similar bonds (Fig. 2e, f). The kinetic off-rate (koff) or dissociation rate is obtained from the intercept of the fit (at LR = 0) yielding koff values of 0.008 ± 0.005 s−1 and 0.009 ± 0.006 s−1 for S1 subunit and RBD, respectively. These values are in good agreement with reported values obtained by surface plasmon resonance for the S glycoprotein (koff = 0.003 s−1)18 and the RBD subunit (koff = 0.008 s−1) binding to ACE2 receptors19.
Assuming that the receptor-bond complex can be approximated by a pseudo-first-order kinetics, we also estimated the kinetic on-rate (kon) from our single-molecule force spectroscopy experiments11 (Fig. 2g, h). This association rate is extracted from the binding probability (BP) measured at various contact times, and depends on the effective concentration described as the number of binding partners (ligand + receptor) within an effective volume Veff accessible under free-equilibrium interaction. Veff can be approximated by a half-sphere with a radius including the linker, the viral glycoprotein (S1 subunit or RBD) and the ACE2 receptor. For both the S1 subunit and RBD, we observed that the binding frequency increased exponentially with contact time, and we extracted an interaction time of ~0.250 ms, leading to a kon of 6.4 × 104 M−1 s−1 and 8.0 × 104 M−1 s−1, respectively. Finally, the dissociation constant KD is calculated as the ratio between the koff and the kon, yielding values around ~120 nM for both complexes. This value corresponds to a high-affinity interaction, confirming the specificity of the complexes established by SARS-CoV-2 with the ACE2 cell-surface receptor, which in turn results in a long lifetime of the virus attachment to the cell surface. Other interaction studies between SARS-CoV (80% sequence homology to SARS-CoV-2) and ACE2 reported specific, high-affinity association values also in the nM range20. For comparison, a variety of examples for low- as well as high-affinity interactions between other virus-receptor pairs are summarized in Dimitrov et al.21 and include influenza A—SA (mM) or HIV-1—CD4 (nM) interactions. For single-molecule interactions, the bond lifetime τ can be directly related to the inverse kinetic off-rate (τ = koff−1), resulting here in a τ of 125 ms for the S1 subunit and 111 ms for the RBD, respectively. Of course, at the virion level, the overall bond lifetime will increase with the multivalence of the interaction. By definition, high-affinity interaction has a long lifetime as the dissociation constant KD is defined as the ratio between koff and kon. For high-affinity interactions, the KD is in the nM range, leading to koff « kon and therefore maintaining the interaction in its bond state for very long times, making the development of anti-binding molecules targeting this interaction more difficult. Finally, we also used optical biolayer interferometry (BLI) to confirm the kinetic parameters characterizing this interaction, and obtained very close affinities in the same nM range as AFM experiments (Supplementary Fig. 5). Taken together, our in vitro experiments confirm that SARS-CoV-2 binding to the ACE2 receptors is mediated by the RBD–ACE2 interface as our experimental conditions did not highlight any significant difference between S1 subunit and RBD binding.
Validation of the interaction on living cells
Next, we wanted to investigate whether the interaction probed on isolated receptors is also established in physiologically relevant condition. To this end, we performed binding assays on living A549 cells (human adenocarcinoma alveolar basal epithelial cells). While this cell line is widely used as a type II pulmonary epithelial cell model, it has been shown recently that those cells are incompatible with SARS-CoV-2 infection22. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Although undifferentiated cells (cultured at low confluency) only express little ACE2, overexpression of ACE2 in undifferentiated A549 cells facilitated virus entry23. We transiently transfected ACE2–eGFP in A549 cells (A549–ACE2) and probed S1-subunit binding to those cells as well as to A549 cells (serving as internal control) (Fig. 3a and Supplementary Fig. 6). Confocal images showed ACE2–eGFP receptors homogeneously distributed in small domains at the surface of A549 cells (Fig. 3b). Guided by fluorescence (Fig. 3c), we chose areas in which both cell types, i.e., transfected (A549–ACE2, green fluorescence) and nontransfected (A549, no fluorescence) cells, were in proximity to one another. Having both A549 cell types in one image area served as a direct control to evaluate whether interactions measured by the functionalized tip were indeed due to specific binding to fluorescent ACE2–eGFP receptors, and to evaluate the extent of other types of interactions (Fig. 3c–e). In such area, we simultaneously recorded a height image (Fig. 3d) and the corresponding adhesion map (Fig. 3e), which were reconstructed from FD curves recorded for each topographic pixel. The retraction part of FD curves showed specific adhesion events mainly on A549–ACE2 cells, with a significantly higher BP (Fig. 3f), as exemplified with the presented adhesion map that shows 20.1% of adhesive pixels on the A549–ACE2 cell versus 13.5% on the control cells (Fig. 3e and Supplementary Fig. 7). Specific binding forces (and corresponding LR) were extracted from force vs. time curves recorded on A549–ACE2 cells (Fig. 3g) and overlaid on the DFS plot obtained on purified ACE2 receptors (Fig. 3h). To explore a wide range of LR, we probed the interaction at various frequencies and amplitudes (see Methods). We observed a very good alignment between the data obtained on purified receptors and on living cells confirming the physiological relevance of our results obtained on model surfaces.
Fig. 3: Probing S-glycoprotein binding to the ACE2 host receptor on living cells.

a Binding of S-glycoprotein subunit 1 (S1) is probed on A549 and A549–ACE2 cells.
b Confocal microscopy (z stack) of A549–ACE2–eGFP (green) cell transduced with plasma membrane BFP (blue).
c Overlay of eGFP and DIC images of a mixed culture of A549 and A549–ACE2–eGFP cells.
d, e Force–distance (FD)-based AFM topography image (d) and the corresponding adhesion map (e) in the specified area in (c). The frequency of adhesion events is indicated.
f Box plot of the binding probability between S1 and A549 cells (gray) or A549–ACE2 cells (green) without and after injection of cyclic RGD (cRGD, checked boxes) or sialic acid (SA, dashed boxes), respectively. The square in the box indicates mean, the colored box indicates the 25th and 75th percentiles, and the whiskers indicate the highest and the lowest values of the results. The line in the box indicates median.
g Force versus time curves showing either a nonadhesive curve (bottom) or specific adhesive curves acquired at different LRs (LR1–LR3).
h DFS plot showing the distribution or the rupture forces measured either between the S1 subunit and the ACE2 on model surfaces (black dots, extracted from Fig. 2e), and between the S1 subunit and ACE2-overexpressing A549 cells acquired at three different LRs (blue and red dots) (N = 403). Blue dots belong to a data set acquired in fast-force volume mode, with a retraction velocity of 20 µm s−1 (LR1). Red dots belong to data sets acquired in peak force tapping mode with 0.125 kHz peak force frequency and 375-nm amplitude (LR2) or at 0.25 kHz and 750 nm (LR3), respectively. The error bar indicates s.d. of the mean value. Histograms of force distribution on A549–ACE2 cells for LR1–LR3 are shown on the side. For experiments without injection of cRGD or SA, data are representative of at least N = 11 cells from N = 6 independent experiments. The data for blocking experiments with cRGD or SA were acquired for at least N = 4 cells from N = 2 independent experiments. P values were determined by two-sample t test in Origin. Source data are provided as a Source Data file.
S1 subunit binding to the cell involves other receptors
Our FD-based AFM experiments performed on living cells put in evidence that the S1 subunit interacts even on control cells with a frequency ≈10% although the expression level of ACE2 should be very low as the cells are not differentiated. Nevertheless, some evidence pointed out that human CoV S glycoproteins possess sialic acid (SA)-binding sites and in particular to 9-O-acetyl-sialogycans24, and that integrins could also be a receptor for the SARS-CoV-2 (ref. 25), which possesses a RGD motif close to the ACE2-binding site. To evaluate whether these other receptors could be involved during the early binding steps to the cell surface, we performed additional experiments by injecting 9-O-acetyl-sialogycans to block interaction with cell-surface SA, or added cyclo-RGD (cRGD) to compete with the interactions with integrins. After SA injection, the binding frequency was reduced on A549 cells down to ~7% and to ~10% on ACE2-transfected cells (Fig. 3f and Supplementary Fig. 8). For integrins, injection of cRGD only reduces the binding frequency of ~1–2% on both cell types, which is in good agreement with the fact that integrins are mostly expressed on the bottom of the cell26. Altogether, these data obtained on cells by AFM represent to date the best evidence that S1–ACE2 complex is established in physiologically relevant conditions and underlines the complex situation with multiple cell-surface receptors accounting for the whole interaction.
Inhibition of S1-subunit binding using ACE2-derived peptides
Human recombinant soluble ACE2 (hrsACE2) is currently being considered for treatment of COVID-19 (refs. 27,28). However, ACE2 is involved in many key cellular processes, such as blood-pressure regulation and other cardiovascular functions. Therefore, hrsACE2 treatment could lead to dysregulation of those vital processes and subsequently cause deleterious side effects for treated patients. To avoid any interference of the ACE2 homeostasis, we wanted to test whether small ACE2-derived peptides can also interfere with SARS-CoV-2 binding, by blocking binding sites on the S glycoprotein. To this end, we synthetized four different peptides (sequences provided in Supplementary Fig. 9), which have been selected to mimic the regions of ACE2 that interact with the S1 subunit as determined by the crystal structure29, and we tested their binding inhibition properties using our single-molecule force spectroscopy approach (Fig. 4a, b). We first measured the BP between the S1 subunit and the ACE2 in the absence of peptide (0 µM), with a contact time of 250 ms, as reference, and then injected our ACE-derived peptides at three different concentrations (1, 10, and 100 µM). For the four peptides, we observed a progressive reduction of the BP as a function of the concentration confirming a specific inhibition. In addition, for each peptide, we noticed a reduction of >50% of the probed interactions already for the 1–10 µM concentration, suggesting a 50% inhibitory concentration (IC50) in the µM range. The [22–44] peptide shows the highest inhibition of the S1–ACE2 complex formation with a measured reduction in the BP of ~76%. The [22–57] peptide shows a similar inhibition potential (~74%), suggesting that the additional amino acids do not influence the overall affinity of the peptide for the S1 subunit, as also confirmed by molecular dynamics (MD) simulations showing that although the peptide 22–57 is longer, less H bonds are established between the peptide and the RBD domain (Supplementary Fig. 10). Overall, these results are in good agreement with the structural insights because these peptides are derived from the N-terminal helix of the ACE2 and therefore form with the RBD interface an important network of hydrophilic interactions (including nine hydrogen bonds and a salt bridge). Within the ACE2–RBD complex, the [351−357] fragment is also part of a “hot binding spot” that results in our test by a good score with a reduction of ~60% of the initial specific BP. Finally, the [22–44–g–351–357] peptide was also synthetized and tested based on the fact that in the crystal structure, the distance between S44 and L351 is close enough to be filled by a single amino acid. A glycine residue was added between the two fragments because the two ACE2 fragments have opposite directionality, and glycine has a high propensity to form reverse turns. Nevertheless, under our experimental conditions, we did not notice any strong improvement in the binding inhibition. Altogether, our in vitro assays at the single-molecule level provide direct evidence that ACE2-derived peptides are strong candidates to potentially inhibit SARS-CoV-2 binding to ACE2 receptors (Fig. 4c).
Fig. 4: Anti-binding effects of ACE2-derived peptides on S1-subunit binding.

a Efficiency of blocking peptides is evaluated by measuring the binding probability of the interaction between the S1 subunit and ACE2 receptor on model surface before and after incubation of the functionalized AFM tip with the four different peptides at increasing concentration (1–100 µM).
b Histograms, with the corresponding data points overlaid in dark gray, showing the binding probability without peptide (0 µM) and upon incubation with 1, 10, or 100 µM of ACE2-derived peptides ([22–44], [22–57], [22–44–g–351–357], and [351–357]). The binding probability measured with a polyethylene glycol (PEG) tip enables to evaluate the nonspecific binding level. The prediction of the structure of the ACE2-derived peptides is shown in the inset. The structure of the peptides is based on the structure of the peptide in the crystal structure (PDB ID: 6m0j). For the [22–44–g–351–357] peptide, its structure was generated using homology modeling41. The error bar indicates s.d. of the mean value.
c Graph showing the reduction of the binding probability. Control with ddH2O is provided in the inset showing that repetitive measurements do not result in a similar decrease of the binding probability. Data are representative of at least N = 3 independent experiments (tips and sample) per peptide concentration. P value was determined by two-sample t test in Origin. The error bar indicates s.d. of the mean value. Source data are provided as a Source Data file.
ACE2-derived peptide blocks specific binding to living cells
Finally, we tested whether the [22−57]-binding inhibition peptide could also prevent S1-subunit binding in the cellular context (Fig. 5). The interaction between the S1 subunit and the confluent layer of a coculture of A549 and A549–ACE2 cells was probed before and after addition of the peptide at 100 µM. Before injection, cells overexpressing the ACE2 receptors (A549–ACE2) show higher BP (9.4 ± 1.6% vs. 19.4 ± 7.3%, for A549 and A549–ACE2, respectively) (mean ± S.D., N = 4) (Fig. 5a–d), in good agreement with our previous observation (Fig. 3f). After injection of the [22−57] ACE2-derived peptide, we observed a significant decrease of the BP on both cell types (Fig. 5e, f). In particular, the BP on A549–ACE2 cells significantly drops (~70%), reaching a level close to the one of the control cells. Taking into account that undifferentiated A549 cells express little ACE2 and are poorly infected by CoV23, this result supports the biological relevance of our ACE2-derived peptide acting as potential inhibitor capable of efficiently blocking SARS-CoV-2 binding.
Fig. 5: Blocking of S1-subunit binding using ACE2-derived peptide on living cells.

a Box plot showing that the reduction of binding probability measured the S1-subunit-derivatized tip and a mixed culture of A549 and A549–ACE2 cells upon injection of the [22–57] ACE2-derived peptide. The square in the box indicates mean, the colored box indicates the 25th and 75th percentiles, and the whiskers indicate the highest and the lowest values of the results.
b Overlay of eGFP and DIC images of a mixed culture of A549 and A549–ACE2–eGFP cells. FD-based AFM topography images (c, e) and the corresponding adhesion map (d, f) recorded in the specified area in (b) (scanned with a scan angle) before (c, d) and after (e, f) incubation of the tip with the [22–57] ACE2-derived peptide. The frequency of adhesion events is indicated. Data are representative of at least N = 4 cells from N = 2 independent experiments. P values were determined by two-sample t test in Origin. Source data are provided as a Source Data file.
In conclusion, we investigated the interaction established between the SARS-CoV-2 S glycoprotein and the ACE2 receptor using single-molecule force spectroscopy. We demonstrated a specific binding mechanism between the S1 subunit and the ACE2 receptor. By comparing the binding of the S1 subunit and the RBD toward the ACE2 receptor, our experiment evidenced that both domains interact with the same kinetic and thermodynamic properties toward the ACE2 receptor, highlighting that SARS-CoV-2 binding to ACE2 is dominated by the RBD/ACE2 interface. Our measurements show that under our physiologically relevant conditions, the RBD binds the ACE2 receptor with an intrinsic high affinity (~120 nM), which could even be further stabilized at the whole-virus level, thanks to possible multivalent bonds between the S-glycoprotein trimer and ACE2 dimer.
Based on the available crystal structures of the molecular complex, we examined how several ACE2-derived peptide fragments could interfere with the S1–ACE2 complex formation. While all tested peptides show binding inhibition properties, peptides mimicking the N-terminal helix of the ACE2 receptor show the best results. Both [22–44] and [22–57] peptides exhibit an anti-binding activity with IC50 in the µM range, resulting in a >70% decrease in the BP observed by AFM on purified receptor and >70% on living cells. On the cellular model, we observed that the BP drops to the level of the control cells (undifferentiated A549 cells) that are poorly infected by CoV23. Therefore, those peptides appear as strong therapeutic candidates against the SARS-CoV-2 infection.
Methods
Cell culture and transfection
A549 cells (ATCC® CCL-185) were grown in Ham’s F-12 Nutrient Mix with 10% fetal bovine serum, penicillin (100 U ml−1), and streptomycin (100 µg mL−1) (Gibco) at 37 °C in a humidified atmosphere with 5% CO2. pcDNA3.1(+) ACE2–eGFP was transfected using Lipofectamine LTX (Invitrogen) according to the manufacturer’s protocol. In brief, 2 μg of pcDNA3.1(+) ACE2–eGFP was transfected to A549 cells (60-mm plate) using 6 μl of Lipofectamine LTX and 2 μl of PLUS reagent (Invitrogen).
Functionalization of AFM tips
PFQNM-LC and MSCT-D cantilevers (Bruker) were used to probe the interaction between S1 subunit (Genscript, #U5377FC120) or RBD protein (Genscript, #U5377FC120) and ACE2 protein (Sino Biological, 90211-C02H). NHS-PEG24-Ph-aldehyde linkers were used to functionalize AFM tips as previously described30. Briefly, the cantilevers were immersed in chloroform for 10 min and further cleaned in a UV radiation and ozone (UV-O) cleaner (Jetlight), and immersed overnight in an ethanolamine solution (3.3 g of ethanolamine in 6.6 ml of DMSO). They were washed with DMSO and ethanol three times, respectively. Ethanolamine-coated cantilevers were immersed in NHS-PEG24-Ph-aldehyde solution (3.3 mg of it was diluted in 0.5 ml of chloroform and 30 μl of triethylamine) and finally washed 3 times with chloroform and dried with nitrogen.
For AFM tips functionalized with S1-subunit protein, 50 µl of S1-subunit protein solution (0.1 mg/ml) was put onto the cantilevers placed on Parafilm (Bemis NA) and 2 µl of fresh NaCNBH3 solution (6 wt% vol-1 in 0.1 M NaOH(aq)) was mixed in the protein solution. The cantilevers were incubated in the solution for 1 h on ice. Then, 5 µl of 1 M ethanolamine solution was carefully added to the protein solution and incubated 10 min to quench the reaction and finally washed three times with PBS.
For AFM tips derivatized with the RBD protein, 100 µl of a 100 µM tris-nitrilotriacetic amine 540 trifluoroacetate (Toronto Research Chemicals, Canada) (tris-NTA) solution was put onto them placed on Parafilm, and 2 µl of fresh NaCNBH3 solution was mixed in the protein solution. They were incubated in the solution for 1 h on ice. Then, 5 µl of 1 M ethanolamine solution in the protein solution was added and incubated for 10 min. The mixture of 50 µl of RBD solution (0.1 mg ml−1) and 2.5 µl of 5 mM NiCl2 were put onto them and they were incubated for 2 h. After incubation, they were washed in PBS solution three times.
Preparation of ACE2-coated model surfaces
ACE2 protein (Sino Biological, 90211-C02H) was immobilized using NHS–EDC chemistry. Gold-coated surfaces were first rinsed with ethanol, dried with a gentle stream of nitrogen gas, cleaned for 15 min by UV and ozone treatment (Jetlight), and incubated overnight in an alkanethiol solution (99% 11-mercapto-1-undecanol 1 mM (Sigma Aldrich) and 1% 16-mercaptohexadecanoic acid 1 mM (Sigma Aldrich) in ethanol). The chemically activated samples were rinsed with ethanol, dried with nitrogen gas, and immersed for 30 min in the solution of 100 mg of chemically activated dimethylaminopropyl carbodiimide (Sigma Aldrich) and 40 mg of N-hydroxysuccinimide in 4 ml of milliQ water. Finally, the surfaces were rinsed with milliQ water, incubated with ACE2 protein (0.1 µg µL−1 in PBS) on Parafilm (Bemis NA), and washed in PBS.
FD-based AFM on model surfaces
FD-based AFM on model surfaces was performed in PBS at room temperature using functionalized MSCT-D probes (Bruker, nominal spring constant of 0.030 N/m and actual spring constants calculated using thermal tune)31. A Bioscope Resolve AFM (Bruker) operated in the force–volume (contact) mode (Nanoscope software v9.1) was used. Areas of 5 × 5 µm were scanned, ramp size set to 500 nm, and set point force of 500 pN, with a resolution of 32 × 32 pixels and a line frequency of 1 Hz.
DFS analysis (using a constant approach speed of 1 µm/s and variable retraction speeds of 0.1, 0.2, 1, 5, 10, and 20 µm/s) and kinetic on-rate estimation (measuring the BP for different hold times of 0, 50, 100, 150, 250, 500, and 1000 ms) were performed. Regarding DFS experiments, data including LRs and disruption forces were extracted using Nanoscope analysis (v2.0, Bruker). Origin software (OriginLab) was used to display the results in DFS plots to fit histograms of rupture force distributions for distinct LR ranges, and to apply various force spectroscopy models, as described8,16. For kinetic on-rate analysis, the BP (fraction of curves showing binding events) was determined at a certain hold time (t) (the time the tip is in contact with the surface). Those data were fitted and KD calculated as described previously32. In brief, the relationship between interaction time (τ) and BP is described by the following equation:
(1)
where A is the maximum BP and t0 the lag time. Origin software is used to fit the data and extract τ. In the next step, kon was calculated by the following equation, with reff the radius of the sphere, nb the number of binding partners, and NA the Avogadro constant
(2)
The effective volume Veff (4πreff3) represents the volume in which the interaction can take place. This results in a half-sphere, since only half of the S1 molecules can interact with its corresponding receptor on the substrate.
Peptides and competition-binding assays
To assess the influence of peptides on the S1-subunit–ACE2 interaction, binding probabilities were measured before and after tip incubation with 1, 10, and 100 µM of peptide. Briefly, a first map was recorded as described above (i.e., force-volume mode, 1 µm/s approach and retraction speed, ramp size of 500 nm, an applied force of 500 pN, resolution of 32 × 32 pixels, line frequency of 1 Hz, and hold time of 250 ms), then the peptide at the appropriate concentration was injected, and a new map was recorded.
All the peptides ([22–44], [351–357], [22–57], and [22–44–g–351–357]) were synthesized by Genscript (Hong Kong). Those peptides are designed according to the sequence of the ACE2 receptor in complex with the RBD domain of the S1 glycoprotein.
FD-based AFM and fluorescence microscopy on living cells
An AFM (Bioscope Resolve, Bruker) coupled to a confocal microscope (Zeiss LSM-980) was used to acquire correlative images. The AFM was equipped with a 150-µm piezoelectric scanner. The AFM and the microscope were equipped with a cell-culture chamber allowing maintaining the temperature (37 ± 1 °C). To keep cells alive, the humidified (95 ± 2% relative humidity) synthetic air (80% N2 and 20% O2) was supplemented with 5% CO2 and filled continuously around the cell plate allowing to diffuse into cell-culture media16. Fluorescence images were recorded using a water-immersion lens (×63, NA 1.20, Zeiss C-Apochromat). PFQNM-LC cantilevers (Bruker) were used to record AFM images (~25 μm2) at imaging forces of ~500 pN. The cantilevers were oscillated either at 0.25-kHz peak force frequency with a 750-nm amplitude, 0.125 kHz with a 375-nm amplitude in the PeakForce Tapping mode, or at 20 μm s−1 retraction speed in fast-force-volume mode. The sample was scanned using 256 pixels per line (256 lines) and a frequency of 0.125 Hz. To study the involvement of other receptors, cells were treated with either 1 mM of 9-O-acetyl-sialogycans or 500 μM of cRGD. AFM images and FD curves were analyzed using Nanoscope analysis software, Origin, Gwyddion, and ImageJ. Optical images were analyzed using Zen software (Zeiss). The fluorescence intensity was measured with Zen software (Zeiss). The same size of the area was taken on A549–ACE2 and A549 cells. The average intensity of the area was calculated with Zen software. The statistical analysis was performed with Prism (Graphpad).
Plasma membrane staining
Plasma membrane-CFP BacMam 2.0 (Invitrogen) was used to check the co-localization of ACE2 protein and plasma membrane according to the manufacturer’s protocol. In brief, 2 μl of plasma membrane-CFP BacMam 2.0 per 10,000 cells was added on the cell-culture dish 16 h (37 °C) before imaging. Z-stack image was recorded by confocal LSM-980 (Zeiss) using a water-immersion lens (×63, NA 1.20, Zeiss C-Apochromat) and 445- and 488-nm laser line.
Affinity measurements using BLI
Affinity between the S1 subunit or RBD and ACE2 was also investigated by BLI, using a Blitz® device equipped with amine-reactive second-generation (AR2G) biosensors (Pall ForteBio). After hydrating the biosensor for 10 min and performing an initial baseline (1 min), the biosensor surface was chemically activated (5 min) by a freshly prepared 20 mM EDC and 10 mM NHS (in milliQ water) solution. Then, ACE2 (0.025 µg µL−1 in acetate buffer, pH 4) was loaded onto the biosensor during 3 min and the reaction quenched with ethanolamine 1 M (pH 8). After another baseline step (1 min in PBS), binding of S1 subunit or RBD (0.1 mg mL−1) was measured for 5 min. Finally, the dissociation step (5 min) was performed in PBS. Data processing and analysis were run using a routine provided by GraphPad Prism.
MD simulation between ACE2 peptides and S glycoprotein
The PDB (code: 6m0j)29 was used to perform a MD simulation between ACE2-derived peptides and the SARS-CoV-2 spike protein complex. MD simulations were performed utilizing the Gromacs package33,34 and carried out using the Amber99SB-ILDN35 force fields in TIP3P water36. The simulation system consisted of a peptide, a protein, and water (about 20,000 molecules) in a cubic box that extended 10 nm from the protein. Appropriate amounts of sodium/chlorine ions were added in the system. For starting the simulation, the environment had to be developed as follows. The steepest descent algorithm was performed either up to 50,000 steps or by 100 kJ mol−1 nm−1. Then, the environment of the system changed at 300 K (NVT ensemble) and subsequently at 300 K and 1 bar (NPT ensemble). After developing the environment, the Particle Mesh Ewald37 method was used to calculate the long-range electrostatic interactions. Short-range dispersion interactions were described by a Lennard–Jones potential with the cutoff of 1 nm. After reaching the equilibrium of temperature and pressure, MDs were conducted for 60 ns at 300 K and 1 bar. The LINCS algorithm38 was applied to constrain the covalent bonds with hydrogen atoms. The time step of the simulations was set to 2 fs. The interactions above 10 Å were regarded as nonbond. To determine whether a hydrogen bond exists between a peptide and a protein in the MD models, a geometrical criterion was adopted, in which the formation of a hydrogen bond was defined by both atom distance and bond orientation. For example, assuming donor D, hydrogen H, and acceptor A consists of D–H ··· A configuration. Then when the distance between donor D and acceptor A was shorter than 3.5 Å as well as the bond angle H–D ··· A smaller than 60.0°, it has been regarded as a hydrogen bond. The hydrogen bonds are counted for 55–60 ns while running the simulations.
Synthesis of 9-O-acetyl-2-α-O-propargyl-SC
2-α-O-propargyl SC was synthesized by the protocol described by Dashkan et al.39. This molecule was selectively acetylated at the 9-position following the procedure of Ogura et al.40.
Reporting summary
Further information on research design is available in the Nature Research Reporting Summary linked to this article.
Data availability
The Source data underlying Figs. 2c, e–h, 3f, h, 4b, c, 5a and Supplementary Figs. 2,6, 7 are provided as a Source Data file. All other relevant data are available from the corresponding authors upon reasonable request. Source data are provided with this paper.
Change history
14 May 2021
A Correction to this paper has been published:
https://doi.org/10.1038/s41467-021-23498-x
***
Tuossa Modernan patentin geenipätkässä koronaviruksellakin JA MONELLA MUULLA esiintyvästä FCS (furin cleavage site) -piikkiproteiinista EI OLE MITÄÄN UUTTA EIKÄ LABRASSA "TYHJÄSTÄ TEHTYÄ" EIKÄ MUKA "LUONNOSSA MAHDOTONTA", kuten Dalgleish ja Sörensen NATO-disinformaattorit väittivät, vaan Moderna on vaan onnistunut patentoimaan luonnon geenikoodia (mikä ei ole tarkoitus, mutta sitä "sattuu" niin kauan kuin jotakin geenejä voi jossain patentoida.
Liioin ei mainita mitään, että tämä nimenomainen pätkä olisi jossakin erityisen tärkeässä merkityksessä vaikka tappavuuden kannalta.
https://en.wikipedia.org/wiki/Furin
"
Americas
Questions raised over code in Moderna patent
By HENG WEILI in New York | China Daily | Updated: 2022-03-21 09:52

A vial and syringe are seen in front of a displayed Moderna logo in this illustration taken Jan 11, 2021. [Photo/Agencies]
Part of its genetic sequence mirrors part of genetic sequence in virus, study says
The COVID-19 vaccine produced by Moderna Therapeutics Inc has brought the Massachusetts biopharmaceuticals company billions of dollars in sales, much of that through purchases of its shots by the US government.
But as with other vaccines, the debate over their efficacy and side effects continues, as does the debate over the origin of the specific coronavirus that causes COVID-19.
Moderna, Pfizer-BioNTech and Johnson & Johnson produce the COVID-19 vaccines administered in the United States and most of those used in the European Union.
Now, a study, MSH3 Homology and Potential Recombination Link to SARS-CoV-2 Furin Cleavage Site, by an international team of scientists that was published in Frontiers in Virology last month, has indirectly raised questions about a patent Moderna was awarded in 2017.
The team found that a tiny piece of genetic code in the coronavirus is identical to part of a gene patented by Moderna well before the onset of the COVID-19 pandemic.
The study's scientists said there is a 1-in-3-trillion chance Moderna's sequence randomly appeared through natural evolution, although others said the occurrence could be coincidental.
The lead scientist of the study was Bala Ambati, a research professor at the University of Oregon. The team also included scientists from India, Italy and Switzerland. Scientists affiliated with Michigan State University, the University of Pittsburgh and the University of South Florida were among those who conducted the research.
"Our peer-reviewed article was published as a perspective, the main purpose of which was to stimulate discussion," Ambati told China Daily. "We understood from the beginning that this match could be random chance and stated this in the article very prominently.
"What stimulated our interest was not that the sequence was from Moderna, and not that there were other matches in the BLAST (Basic Local Alignment Search Tool) database, but rather that it matched the reverse complement of a synthetic and likely human codon-optimized MSH3 mRNA.
"This led us to the idea that it was possible that there could have been recombination in a human cell line containing this mRNA and a SARS-like virus to produce the FCS (furin cleavage site). Potential experiments could come from this perspective to test this hypothesis."
Potential experiments
The team's "only interest is seeing if an experiment could be designed to test our hypothesis. If such an experiment resulted in the acquisition of an FCS, especially from a synthetic mRNA sequence, it would be quite interesting. However, there are multiple other hypotheses that propose a lab leak that are supported indirectly, that probably have a better basis at this point than ours."
Ambati said there are also "many hypotheses for a natural spillover which also have reasonable bases as well. The issue with most of these hypotheses is that they are not prospectively testable. We want to stimulate discussion amongst all concerned on both 'sides' of the issue to try to produce prospective experiments that can prove or disprove their hypotheses. That is the major purpose of our perspective paper.
"We did not wish to cast aspersions on any person, company, or country. The genetic sequence was discovered in SARS-CoV-2's (the coronavirus') furin cleavage site (FCS), the part that makes it highly efficient at infecting people and that separates it from other coronaviruses.
"We cannot control social media and what it says. For this reason, we do not participate in it. The proper scientific manner is to write an email to us or a published letter to Frontiers and ask us to respond to it." China Daily's correspondence with Ambati was by email.
The coronavirus shares a sequence of 19 specific letters with the genetic section owned by Moderna, which makes an mRNA COVID-19 vaccine. The "m" stands for messenger.
The study said: "A BLAST search revealed that a 19 nucleotide portion of the SARS-CoV-2 genome encompassing the furin cleavage site is a 100 percent complementary match to a codon-optimized proprietary sequence that is the reverse complement of the human mutS homolog (MSH3).
"In any case, the presence of the 19-nucleotide long RNA sequence including the FCS with 100 percent identity to the reverse complement of the MSH3 mRNA is highly unusual and requires further investigations," the study concluded.
SARS-CoV-2 is the only coronavirus to carry 12 unique letters that allow its spike protein to be activated by the furin enzyme, allowing it to easily spread between human cells. The furin cleavage site is located on the spike protein, the structure that binds to human cells.
SARS-CoV-2 carries all the information needed for it to spread in about 30,000 letters of genetic code, or RNA. RNA is present in all living cells. Its main role is to act as a messenger carrying instructions from DNA for controlling protein synthesis.
Moderna filed for the patent in February 2016 as part of its cancer research division. The sequence is part of the gene called MSH3 that is known to affect how damaged cells repair themselves in the body.
The patent for "Modified polynucleotides for the production of oncology-related proteins and peptides" was awarded by the US Patent and Trademarks Office on March 7, 2017. Scientists have called the pathway a potential avenue for cancer treatments.
Stephane Bancel, the chief executive of Moderna, appeared on Fox Business on Feb 24 and was asked about the international team's findings. "My scientists are looking into those data to see how accurate they are or not. As I have said before, the hypothesis of an escape from a lab by an accident is possible. … Humans make mistakes."
There is some debate about whether the match is as rare as the study claims, with other experts describing it as a "quirky" coincidence rather than a "smoking gun", the Daily Mail of London reported.
Professor Lawrence Young, a virologist at Warwick University in England, said the latest finding was interesting but said it was not significant enough to suggest laboratory manipulation.
,,,,
OHO.
"Tekoäly keksi" uuden koronateorian, joka saattaa kyvinkin olla tosi: kahden vanhastaan tunnetun ihmisellä lieviä oireita aiheuttavan viruskannan risteytys, joka on syntynyt ihmisessä!
https://scitechdaily.com/ai-uncovers-hidden-genetic-clues-that-challenge-covid-19s-origins/
" AI Uncovers Hidden Genetic Clues That Challenge COVID-19’s Origins
By KeAi Communications Co., Ltd.February 11, 2025

Could COVID-19 have originated from a fusion of rare infectious diseases rather than wildlife? A groundbreaking study using AI-driven max-logistic intelligence suggests exactly that.
A surprising new study suggests that COVID-19 may not have originated from bats or pangolins, but rather from a rare fusion of human diseases.
Using an advanced AI-driven approach called max-logistic intelligence, researchers identified genetic links between COVID-19 and two obscure infections — glanders and Sennetsu fever — potentially rewriting the narrative of how the virus emerged.
Unraveling the Origins of COVID-19
The origins of COVID-19 remain uncertain despite extensive research. A new study published in Advances in Biomarker Sciences and Technology (ABST) takes an AI-driven approach to analyze DNA methylation patterns at 865,859 CpG sites in blood samples from early COVID-19 patients.
Led by Zhengjun Zhang from the University of Wisconsin’s Department of Statistics, the study used max-logistic intelligence to identify strong genetic links. The findings suggest that COVID-19 may have resulted from the natural fusion of two rare infectious diseases — glanders and Sennetsu fever
— combined with common human illnesses.
Visualization of site-site relationship and site-risk probabilities. Credit: Zhang, Z.

A Shift Away from Wildlife Origins
This challenges the widely accepted belief that the virus originated in bats or pangolins, raising the possibility that previous studies placed too much emphasis on wildlife origins.
“Establishing such connections across 865,859 CpG sites is quite a challenge, with random correlations occurring at a probability of less than one in ten million,” says Zhang. “However, when factoring in the rarity of these diseases, the odds of discovering a meaningful link drop to just one in one hundred million, further strengthening the validity of these results.”
Max-Logistic Intelligence: A Game Changer?
Max-logistic intelligence has been previously demonstrated in cancer biomarker studies. Unlike traditional AI algorithms or modern machine learning techniques such as random forests, deep learning, and support vector machines, max-logistic intelligence offers greater interpretability, consistency, and robustness, making it especially useful for establishing causal relationships.
Zhang emphasized that while identifying reliable biomarkers is critical for scientific progress, many gene markers identified in isolated studies fail in other cohorts, resulting in low or no cross-group commonality.
“DNA methylation, the process by which methyl groups are added to DNA, plays a central role in gene expression and disease development,” explains Zhang. “Errors in methylation can trigger diseases, prompting studies into COVID-19’s DNA methylation patterns.”
Reference: “Etiological connections between initial COVID-19 and two rare infectious diseases” by Zhengjun Zhang, 9 December 2024, Advances in Biomarker Sciences and Technology.
DOI: 10.1016/j.abst.2024.12.001
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