P681R appears better than P681H in Delta, and the other way around in Alpha.
That
could be a false signal from a founder effect, but after this much time
and selective pressure, I seriously doubt it. It's the other residues
for Delta and Alpha that are most interesting, because P681H alone in
Alpha does little and Delta stinks with H681 or P681.
This
paper reports that Alpha with H681(GISAID accession EPI_ISL_999340) is
more infectious than Delta with P681. Delta with R681 obviously
dominated. Alpha's RBD has 200x the binding affinity for hACE2 as
compared to Delta's RBD.
Unfortunately,
they did not test Alpha with H681R. It is likely that another one of
Delta's mutations is required to make P681R so synergistic, so I no examination of that or synergistic mutations for P681H in Alpha to be a serious
omission from this work, and I've served on enough review panels to say that.
Anyway, I think this is the
main takeaway: antigenic drift is wider than presumed, and haplotypes
linger. Perhaps waiting for the immune response specific to them to
wear off, some strains are more in transmission bottlenecks than they
are en route to extinction, in this case Alpha due to Delta's
superiority today. Alpha and Delta are not far enough apart antigenically for
Alpha to recover yet, and it may still die out, but it should drift far enough eventually.
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