This Newsweek article describes some of the research that Wuhan Institute of Virology conducted on Coronaviruses known as 'gain of function':
External Quote:
What's more, Wuhan Institute of Virology scientists have for the past five years been engaged in so-called "gain of function" (GOF) research, which is designed to enhance certain properties of viruses for the purpose of anticipating future pandemics. Gain-of-function techniques have been used to turn viruses into human pathogens capable of causing a global pandemic......
Newsweek writes "scientists have for the past five years been engaged" and the evidence we have is "five years ago", not "for the past five years", but that's close. This covers the two scientists from WIV being consulting authors on the Chapel Hill study.
Your phrasing is "the WIV conducted", and that's not covered by the Chapel Hill paper, because that research was conducted by the U of NC at Chapel Hill, and the Wuhan institute itself was not involved (but two scientists who work there were).
The difference is that "the WIV conducted" implies that there was GOF research in Wuhan, and that isn't what happened. The Newsweek article tries very hard to create the same impression with their phrasing, but almost manages to stay on the right side of the truth. You don't. Your phrasing was a simplification that was wrong and misleading. Just acknowledge that and move on.
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I shared a link on another GOF paper and you disputed that Insisting it was all about cell culture. That's like saying you are not Canadian, you are a man.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5708621/
Could you demonstrate what elements of a research paper qualify it to be a GOF research and show which elements this particular paper is lacking?
You led this with "Here's another example" (of what?) and I asked "These are cell culture experiments, they're not GOF experiments? What claim do you want this source to prove?" It wasn't clear to me whether you want this paper to be evidence that they're doing animal passage (but it's a cell culture experiment) or whether you think it shows GOF (it doesn't), because that's what we've been discussing; or if you're after something else entirely.
But here's the thing: if YOU want this paper to be evidence that the WIV does GOF research, then YOU have to prove that claim. The paper doesn't have the word "gain" in it a single time, so it's not obvious. YOU need to make the argument that this is GOF research, which means that YOU have to find an authoritative definition of GOF and apply it to this paper and show that that's what they're doing.
The author summarizes this paper as "In addition, we found bat SARSr-CoV strains with different S proteins that can all use the receptor of SARS-CoV in humans (ACE2) for cell entry, suggesting diverse SARSr-CoVs capable of direct transmission to humans are circulating in bats in this cave." They did work to show that these S-proteins can infect cells via the ACE2-receptor, which they demonstrated using the WIV ACE2 cells. Their aim is to document a function that the bat viruses already have, not to change a virus to make it more functional. The research objective is not GOF.
"They collected SARS-Cov-2" is straight up wrong. This is a 2017 paper, any reference to SARS-CoV is to the 2003 epidemic virus, which differs a lot from SARS-CoV-2. They didn't collect SARS-CoV either, they collected SARSr-CoV, which are "SARS-related coronaviruses".
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Those are not ten generations of ferrets but ten ferrets in different cages.
My words were "This virus must have been
bred from a
very similar virus in
animals for
many generations." Grammatically, we can shorten this to "this virus must have been bred for many generations". This does not involve generations of ferrets, but generations of viruses. You need a new ferret for each generation, so it's not just "ten ferrets in different cages" that you could infect simultaneously and see what happens, you have to infect them one after the other so you get a new generation of the virus for each animal, therefore 10 generations.
The term "prolongued passage" in the nature letter is linked to a study from Tottori, Japan and Wisconsin:
After 24 consecutive passages by air sac inoculation, followed by five passages in chicken brain, the avirulent virus became highly pathogenic in chickens
Fouchier was studying the avian influenza A/H5N1 in his ferrets. Influenza viruses mutate faster than coronaviruses.
Over in the other thread (
https://www.metabunk.org/threads/cl...hors-other-man-made-claims.11103/#post-238095 ), we've been discussing
https://www.biorxiv.org/content/10.1101/2020.03.30.015008v1 , which states that it takes
~40 years of mutation to get from RaTG13 to SARS-CoV-2 -- and RaTG13 is the closest match that we've found so far.
Specifically, SARS-CoV-2 seems to have a mutation rate of less than 25 mutations per year, whereas the seasonal flu has a mutation rate of almost 50 mutations per year.
Given that the SARS-CoV-2 genome is almost twice as large as the seasonal flu genome, it seems as though the seasonal flu mutates roughly four times as fast as SARS-CoV-2.
So if you wanted to do the same type of animal passage GOF research in Wuhan that Fouchier did in the Netherlands, you'd need 40 animals (which species?) that develop an immune reaction to this virus, and with the incubation period and time for the infection to develop and natural selection to do its thing, I estimate at least 2 weeks per generation, so 80 weeks at least.
If you're taking the 29 passages in chickens as benchmark, we might be looking at ~120 coronavirus generations, taking ~240 weeks, so about 5 years.
We know that the WIV has good international connections to other virologists around the globe, Australia, Texas, North Carolina, Berlin. I know that researchers like to talk amongst each other about their projects. I absolutely can't imagine that Dr Shi would have kept a project as big and as long as this a secret while it was ongoing. Some of her international colleagues would know. But nothing in the current situation indicates that they do.
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The nature letter was written by a group of virologists from the US, the UK, and Australia. My quote is heavily excerpted, I'm not indicating elisions.
1. Natural selection in an animal host before zoonotic transfer
This clearly shows that the SARS-CoV-2 spike protein optimized for binding to human-like ACE2 is the result of natural selection.
For a precursor virus to acquire both the polybasic cleavage site and mutations in the spike protein suitable for binding to human ACE2, an animal host would probably have to have a high population density (to allow natural selection to proceed efficiently) and an ACE2-encoding gene that is similar to the human ortholog.
2. Natural selection in humans following zoonotic transfer
Sufficient opportunity could have arisen if there had been many prior zoonotic events that produced short chains of human-to-human transmission over an extended period.
Further serological studies should be conducted to determine the extent of prior human exposure to SARS-CoV-2.
3. Selection during passage
In theory, it is possible that SARS-CoV-2 acquired RBD mutations (Fig. 1a) during adaptation to passage in cell culture, as has been observed in studies of SARS-CoV11. The finding of SARS-CoV-like coronaviruses from pangolins with nearly identical RBDs, however, provides a much stronger and more parsimonious explanation of how SARS-CoV-2 acquired these via recombination or mutation19.
New polybasic cleavage sites have been observed only after prolonged passage of low-pathogenicity avian influenza virus in vitro or in vivo17. Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of a progenitor virus with very high genetic similarity, which has not been described. Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described.
In short, to create SARS-CoV-2 via animal passage, you'd have to find a lab animal where natural selection works to make the bat virus more efficient for humans, and nobody's done that before. You'd need to start with a virus that's close to SARS-CoV-2 so you don't take 40 years to do it, and nobody's seen a virus like that. And then you'd still need to run the equivalent of 29 chicken influenza passages, so ~120 coronavirus passages, which takes years.
What we do know is that people in the villages near the bat caves have bat-cov antibodies, which means 2 can't be ruled out (and people should probably stop going into bat caves repeatedly to hunt them).
So, to summarize this letter:
- SARS-CoV-2 could've entirely evolved in animals, we see one part in pangolins, another part in bats, they come together sometime and we get Covid. This is likely.
- SARS-CoV-2 could've evolved in a back-and-forth selection via human bat hunters. This is unproven and needs more research.
- SARS-CoV-2 could only have evolved in a lab if we assume several leaps in research that all would have been publishable in their own right, but weren't, and would have taken a very long time project running in secret. This is quite improbable.
To attack this evidence, you need to show that the WIV has made these leaps in research.
You would have to provide a strong motivation to keep this reasearch a complete secret for a long time, in an academic field where there is strong incentive for researchers to publish their findings, and for a group of researchers who have close contact with many colleagues across the world.
The letter has been published on the 17th of February on virological.org and on the 17th of March in Nature, and no such counterevidence has been forthcoming.
This is strong evidence that this virus evolved naturally, and it is also strong evidence that it did not evolve in the Wuhan Institute of Virology.
To question this, you have to either discover new evidence (hasn't happened), or you have to assume a number of unlikely things that we have no evidence for, in the face of a likely explanation that we do have evidence for. In short, this question is not driven by evidence, but rather
by wishful thinking that assumes the worst of fellow humans without any evidence to back it up.
The bold part is why conspiracy theorists are often depressing me.