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I agree with Trevor on this assessment, however, a couple of points: 1. Frequency differences could be entirely due to early seeding with D, followed by later (larger) seeding with G. 2. Differences in Ct values can be due to later testing being better [note trvrb's blog tho].https://twitter.com/trvrb/status/1257825352660877313 …
As Trevor mentions - here and on his blog - there are many confounders (including unknowns) that are not accounted for in the analyses by Korber et al. that could explain the observed differences. Plausible, but far from proven - and I believe the Korber conclusions, premature.
One final note - the change from D>G is predicted to be quite disruptive to quaternary protein structure and we have some hints from flu that these mutations may be functional. E.g.,https://www.ncbi.nlm.nih.gov/pubmed/24368278
Thanks Kristian. Indeed very tricky. And a similar situation to your work on GP A82V in Ebola. In that case there was confounding with Sierra Leone introduction.
Yup, the epi data from the A82V study was so confounded that it was inconclusive (the epi data here, less so). Importantly the Ebola study had experimental data to support a role for A82V in increasing infectivity of human cell, but did that affect transmission? Probably not.
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