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!
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.
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.
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:
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.
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