Paper out in Nature Comms. We developed a framework to analyse the contribution of #SARSCoV2 mutations to the virus' transmissibility. We applied it to nearly 50k genomes and we found none (zero, zilch, nada) that increases transmission!
1/
https://www.nature.com/articles/s41467-020-19818-2
To test if mutations increase transmission of the virus carrying them, we modelled whether, after a mutation emerges, descendants of that virus outperform sister lineages without that particular mutation.
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https://www.nature.com/articles/s41467-020-19818-2
Mutations that are fairly common all seem neutral for the virus carrying them. This includes D614G, which according to our analysis is more of a stowaway that got a lucky ride on a successful lineage, rather than a driver of transmission.
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https://www.nature.com/articles/s41467-020-19818-2
This raises the question why #SARSCoV2 is so well adapted for transmission in humans. A plausible answer is that we missed the early window when it adapted to humans. For more, and about what happened when it later jumped into minks, see:
5/ https://twitter.com/BallouxFrancois/status/1328619165410799619
So, did we waste our time developing and optimising a framework to identify mutations that increase viral transmission, and that detected none? Not necessarily, the imminent arrival of vaccines will exert new selective pressures on #SARSCoV2.
6/ https://twitter.com/BallouxFrancois/status/1331042659230773248
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