Quote:
Originally Posted by Fuzz
DiracSpike, I went back and re-read the article you linked that re-started this discussion:
https://thebulletin.org/2021/05/the-...-box-at-wuhan/
He refers to Andersen, which is what I had posted last year, and explains why it is mostly likely not man made:
https://www.sciencenews.org/article/...nalysis-nature
Now, Wade is a science writer. Andersen is a Professor Department of Immunology and Microbiology. So just off the bat, I'm going to have to but more weight in Andersen, for obvious reasons. He sounds imminently more qualified to discuss the complexities:
https://www.scripps.edu/faculty/andersen/
So I'm not prepared to figure out who is correct. But this guy was:
https://medium.com/woodworkers-of-th...y-e68dafba96fd
Now, I'm not sure who he is, but he seems to know what he is talking about. Big big caveat there, though, since he is anonymous. So if you have another source from a person who identifies their qualifications, I'd be happy to read it. In the mean time, before you take the word of the science writer over the immunologist, I suggest reading through this post, as it seems to point out that Wade doesn't really understand most of what he is saying. |
Hey so I read that Medium article. On the nitty gritty virology stuff I'm really struggling to understand what this guy is disproving about what Wade said.
Quote:
Then Wade tried to falsely characterize one of Anderson’s arguments:
…they [Anderson et al] say that the spike protein of SARS2 binds very well to its target, the human ACE2 receptor, but does so in a different way from that which physical calculations suggest would be the best fit. Therefore the virus must have arisen by natural selection, not manipulation…
This is a major misrepresentation and oversimplification of Anderson’s argument. The S protein shows strong binding affinity for the human ACE2 protein, but ALSO to ACE2 proteins from other species. The viral S protein evolved in a way that bound well, but not optimally to human ACE2. Any synthetic S protein would have been engineered specific to human ACE2, and the binding would have been much more “tailored”.
What Anderson actually said was:
…SARS-CoV-2 …binds with high affinity to ACE2 from humans, ferrets, cats and other species with high receptor homology… SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal7 and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding7,11. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation…
What Anderson meant was that computational calculations show that the binding between the viral S (spike) protein and the human ACE2 protein are not “ideal” — ideal being what we expect from an engineered S protein.
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He claims that Wade is "oversimplifying" Anderson's argument that the virus could not have been man-made because the binding isn't 100% ideal, but then what I bolded are his words where he states that exact same thing. This guy's argument is what Wade was showing as specious reasoning, the assumption that if this was engineered it would have been 100% ideal. Says who? He also goes on in that article to talk about how this research was to progressively search for the threshold of spillover in the infectiousness of viruses...which is pretty consistent with engineering a non-ideal spike protein.
Wade's point are that the two assumptions virologists trotted out to disprove that this could be human made (non-perfect binding and the lack of one of the industry standard DNA backbones) are in fact, not proof positive of anything. Which I agree with. If this virus DID have a recognized DNA backbone then that would be conclusive proof that was engineered, but that flow of logic doesn't work vice versa.