I've said there was no evidence of recent recombination in SARS-CoV-2. That turns out to not be quite right, though it doesn't affect the receptor binding domain. Rather, the S1/S2 cleavage site of SARS-CoV-2 may have been acquired from an HKU9-like virus in the last few decades.https://twitter.com/arambaut/status/1268695688151523329 …
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Can we say how recent other than more recently than the common ancestor with RaTG13 and before November 2019?
More distant that the common ancestor with RaTG13 - RaTG13 *lost* the RBD, but the ancestor of SARS-CoV-2 and the pangolin CoV likely had it. (this is all Andrew's stuff btw - I haven't actually looked at this question deeply).
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Yea I fully agree with Andrew’s analysis. But RaTG13 still has the ancestral sequence from the end of RBD to S1/S2 (and also ancestral S2). So it should still have the ancestral cleavage site. Suggests to me the furin site acquisition is after the SARS2/RaTG13 lineages split.
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Ah, sorry - the furin site acquisition is still unknown. While RmYN02 has an insertion at the S1/S2 boundary, it isn't actually a polybasic site - it just shows that bat viruses 'mess around' with this part of the protein. Bill's post show how these sites can be gained in bats.
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