The coronaviruses being studied at WIV included RaTG13, one of the closest relatives (96.1% genomic match) to SARS-CoV-2 ever found in the wild.
But a key difference between SARS-CoV-2 and it's wild relatives is the spike protein with affinity for the ACE2 receptor, so it would have had to have evolved through an intermediate host with a human-like ACE2 receptor. For example, ACE2-transgenic lab mice.
This does not itself rule out the wild-origin theory, but no wild host that could explain the missing link from RaTG13 to SARS-CoV-2 has yet been found.
Indeed. So the only reasonable conclusion so far is that we haven't found the reservoir host yet. This may take a while and it may even never happen. If and when we do we will finally be able to make another step in this whole saga.
> If there was GoF being done on the sample (adding of the spike protein to infect humans), that could be the remaining percentage.
I do not believe one bit the only "reasonable conclusion" is it has to be from nature.
Between the lab sample, the outbreak area, the GoF program being run, the timing, history of lab leaks, and the reaction, a lab leak is very reasonable...
I think there may have been a slight misunderstanding here (I'm not particularly familiar with this topic so I may have some concepts mistaken):
> The lab-leak scenario presumes zoonotic jump, too. Just rather than from something in the wild, it's from humanized (ACE2-transgenic) mice
> So the only reasonable conclusion so far is that we haven't found the reservoir host yet.
> I do not believe one bit the only "reasonable conclusion" is it has to be from nature.
If it's discovered that the reservoir host was a mouse in a lab at WIV then "we will finally be able to make another step in this whole saga" in the same way as it being discovered as a wild host. It might be worth reading their comment again.
(Again, I'm not deeply familiar with this topic and may be totally off base; gluing together my personal understanding of the meanings of these words has me arriving at this conclusion. I'm also attempting to clarify someone else's statements so take another grain of salt for that.)
But a key difference between SARS-CoV-2 and it's wild relatives is the spike protein with affinity for the ACE2 receptor, so it would have had to have evolved through an intermediate host with a human-like ACE2 receptor. For example, ACE2-transgenic lab mice.
This does not itself rule out the wild-origin theory, but no wild host that could explain the missing link from RaTG13 to SARS-CoV-2 has yet been found.