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The two are not mutually exclusive. The big question in the issue of the proximal origin of the #coronavirus is its adaptation to the human ACE2 receptor. This means it *must* have been present in another common animal with an orthologous ACE2r. #COVID19 (thread) https://twitter.com/jimgeraghty/status/1246125767311982593
Now, what *is* obvious, and I doubt @jimgeraghty is suggesting this, is that this is not an artificially created virus. In fact, I'd expect an artificially created virus to have much higher affinity to non-human primate ACE2r.
The origin of SARS-CoV is relatively well known (shocker: it's freakin' bats, y'all). The closest bat virus to SARS-CoV-2 is RaTG13, from R. affinis. But it's different – there's evidence that it developed affinity to human-like ACE2r under natural selection.
To be specific: the key residues in the receptor binding domain of SARS-CoV-2's spike protein are novel. They're not previously described residues, but an entirely new configuration. This more or less rules out genetic engineering.
Which is how the issue of an intermediate host comes into play. To get the residues in the spike protein for effective ACE2r binding, there must have been exposure to a host that's 1) abundant, 2) has a very similar ACE2r to humans, 3) close to both humans and bats.
The only candidates for this are 1) pangolins (M.javanica specifically), 2) somewhat further behind: tortoises.
So, where do we stand? We know SARS-CoV-2 is not a bat virus. It's close to one (RaTG13), but its crucial part, the spike protein, is the result of a recombination/evolution event. Why is this important? Because to me, it rules out the release of a 'ready' virus.
It may very well be that RaTG13 was (accidentally) released from a lab (then again, it's endemic). But there's no plausible evidence that SARS-CoV-2 could have ever *existed* in a lab first. It shows evidence of viral recombination under selection in nature, in an abundant host.
The very bottom line: I'm way too familiar with the PRC and former Soviet bioweapons programmes to be under any illusions that loss of samples never happens. But the 'lab escapee' theory fails to explain what is probably the most important feature of SARS-CoV-2.
The 'lab escapee' theory fails to explain why, and how, the receptor binding domain recombined to a novel version highly adapted to the human ACE2 receptor ortholog. And so, I press the big 'X to doubt' on @jimgeraghty's hypothesis here.
