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1. 2020-12-21 13:56 Edward C. Holmes open
   Totally agree. Might be good if DRASTIC were distracted for a while.
2. 2020-12-21 14:04 Kristian G. Andersen open
   Chronic infection seems more likely to me - however, I don't think we can rule out potential epizootic spilling back into humans. But all these mutations certainly look consistent with chronic infection
3. 2020-12-21 14:05 Kristian G. Andersen open
   Bob, from the paper above - really does seem 501 is a key 'transmission' residue. Of course, 501T has also been observed.
4. 2020-12-21 14:05 Andrew Rambaut open
   It wouldn't be a simple epizootic - extensive transmission in mink didn't produce more than a few mutations
5. 2020-12-21 14:06 Kristian G. Andersen
   Mink > rodents > humans - or some weird shit. But yeah, I agree - not consistent with what has been observedin mink and fully consistent with what has been observed in chronic infections.
6. 2020-12-21 14:06 Andrew Rambaut open
   South Africa are really worried about E484K (in conjunction with 501Y)
7. 2020-12-21 14:06 Robert F. Garry open
   Actually might be good to ask about for others that are adapting SC2 to mice - we've got a few groups here as well. Baric got Q493K by passing SC2 in mice. https://www.cell.com/cell/fulltext/S0092-8674(20)31247-2?rss=yes It was Sun et al. got N501Y, Q493H, and K417N. https://www.biorxiv.org/content/10.1101/2020.11.10.377333v1
8. 2020-12-21 14:08 Kristian G. Andersen open
   E484K - yeah, I _do_ wonder if there's some weird synergy going on between mutations here - I have a hard time believing all of this is down to 501 alone. But hey :man-shrugging:
9. 2020-12-21 14:08 Andrew Rambaut open
   They also have K417N in ZA

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