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1. 2021-01-14 14:09 Kristian G. Andersen open
   REALLY????
2. 2021-01-14 14:10 Kristian G. Andersen open
   :zany_face:
3. 2021-01-14 14:10 Edward C. Holmes open
   Yes!!
4. 2021-01-14 14:10 Kristian G. Andersen open
   WOW
5. 2021-01-14 14:11 Kristian G. Andersen
   I still consider it MY (highly speculative!) hypothesis! MINE. MY HYPOTHESIS.
6. 2021-01-14 14:18 Edward C. Holmes open
   It's also in that ABC Australian podcast I did the other the day. But you can have it - I'm not 100% convinced yet. I'm not sure why evolution in individual chronic hosts will lead to convergent evolution for increased transmissibility atthe population scale. A few years ago we did a norovirus modelling study that said this sort of thing was unlikely, but that could easily be bollocks. https://academic.oup.com/ve/article/3/2/vex018/4055728
7. 2021-01-14 14:27 Andrew Rambaut open
   There is no evidence that there is increased transmissibility in either the Brazilian or South African strain.
8. 2021-01-14 14:28 Andrew Rambaut open
   It is clearly fit in the populations it is spreading in.
9. 2021-01-14 14:38 Andrew Rambaut open
   The convergence is possibly for cellular infectivity and immune evasion - all things that will be selected for in achronic infection without sterilising immunity. Strong competition between viruses for cells. However, my assumption has always been that this can only be likely to degrade transmissibility (given it was already transmissible at the beginning). But perhaps there is just a fortunate (for the virus) alignment of a within-host fitness peak and a between host one. And the latter involves too many intermediate steps with negative epistatic effects to reach in a stepwisefashion.

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