Earlier quoted context omitted.
I don't take two lineages to be conclusive evidence of multiple zoonotic events. However, the multiple polytomies for each are not easy to explain away. Have you read Pekar's most recent paper in Science? I raise this in earnest, I'm reading it now. A lot of it follows the preprint, but the update more directly addresses many of the points we're discussing. https://www.science.org/doi/10.1126/science.abp8337 My probl…
I led with "just two mutations" because as far as I can tell, all of Worobey's or Pekar's reasoning starts from the assumption that there was no significant cryptic (unsampled) human spread. If the two lineages were tens of SNPs apart, then I believe that would be a reasonable assumption--it would be hard to explain how the virus could spread in humans long enough to accumulate that many mutations without causing eno…
They don't assume that. See the discussion in Pekar. ("The high extinction rate [...] Failed introductions of intermediate haplotypes are also possible.") The whole point of their epidemiological modeling is to disentangle the likelihood of this happening. (See: "Separate introductions of lineages A and B")
The tMRCA doesn't allow enough time for any deep cryptic spread. The authors show this. It's not assumed.
> We show that it is highly unlikely that SARS-CoV-2 circulated widely in humans earlier than November 2019 and that there was limited cryptic spread, with, at most, dozens of SARS-CoV-2 infections in the weeks leading up to the inferred tMRCA, but likely far fewer.