A single line often inverts meaning once you see what it
answers, so neighbouring messages are always shown.
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(and yeah - dN/dS is shit. Just no point).
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I can certainly see that Doug & Phil increased transmissibility, but that does not explain why B.1.1.7 et al.,which arose later, are doing so well. That may have arisen through an intra-host advantage, but it's obvious that they have an epidemiological scale advantage as well. Clearly they have increased fitness which can only be due to (i)increased transmissibilty in itself....which suggests that there should other key mutations in ORF1ab (?) and/or (ii)immune evasion that enables more refection and hence increases R. Perhaps that deletion in nsp6 is the key?
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Are there *proportionately* more chronic infections? Do we know their overall frequency?
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Definitely needs to be set out here.
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2021-02-21 15:35
Edward C. Holmes
The Chan/Petrosky analysis was that dn/ds suggested that there was NO adaptation to humans. This shows otherwise. We know that this mutation is fixed in all the human samples studied to date, but we don't know about any chains of transmission that died out.
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Hmm. Not sure about this paper - they are using software for detecting genomic selective sweeps using LD, I think.
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But they do then do experimental assays to confirm these computational results. I can't judge how good these are. The bottom-line that there has been a continual adaptive process.
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Yeah, the sweep analyses are shit - can't do that in viral genomes, only sexually reproducing organisms. That said, they DID come across a very very interesting mutation (by chance?) and the experimental data is good
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Yes, it's the experimental data that is interesting.