Surveillence minded folks - worth keeping a close eye on BA.2.75 - lots of spike mutations, probable second generation variant, apparent rapid growth and wide geographical spread... github.com/cov-lineages/p…
Spike mutation-wise its got normal BA.2 mutations + K147E, W152R, F157L, I210V, G257S, G339H, G446S, N460K and reversion of R493Q - none of these individually really flag as that worrying but all appearing together at once is another matter...
...and an old thread on 'what second generation variants are' here - didnt really talk about this at the time but theres now a growing consensus that these could be arising from chronic infections
worth saying its entirely possible this is just growing against a background of BA.2(.12.1) and that it hits the encroaching wall of BA.5 and stalls out... we will see
Full credit to all the sequences submitters who've been finding this around the world, Silcn for flagging to pango and @LongDesertTrain@siamosolocani@nzm8qs and @shay_fleishon who've been helping monitor it the past few weeks.
Delighted to be a small part of this new consortium trying to work out what on earths been going on with H5N1 avian influenza viruses the last few years!
Some context - the last few years have seen mass wild bird die offs and some of the highest numbers of jumps into poultry farms ever seen across Europe (in particular in the UK) nature.com/articles/d4158…
At the moment we're really not sure why - theres evidence a new genotype of H5N1 has taken over but its not clear if this is directly causing these outbreaks, or there are other factors that could explain the situation.
Been a hectic month but we had some new SARS-CoV-2/Omicron preprints out in the last few weeks! going to do a 'quick' thread of some of the highlights from these recent studies...
First off we updated our Omicron entry preprint: biorxiv.org/content/10.110…
Headline is - in our hands the entry pathway and antigenicity of Omicron are completely independently encoded by different domains of Spike
As others have seen, in hamster Omicron (BA.1 and BA.2) is pretty apathogenic, whereas Delta/Alpha/early strains cause a lot of weight loss.
Stray thought on what the next variant ('Pi/Rho/Tau') might look like (assuming it eventually comes along).
Heard a few people say 'the only thing we know for sure is it wont look like Omicron' - I think this is largely correct on one level, but maybe an oversimplification...
...I suspect, superficially, the next variant *might* look quite a bit like Omicron - similar numbers of mutations at similar/same amino acid positions - at first glance it might be quite hard to tell apart from Omicron mutation-wise...
...by definition the RBD sites Omicron mutates must be mutationally flexible - I think theres a good chance many of the same sites will also mutated in 'Pi/Rho/Tau' (though mostly with diff substitutions).
Obviously this virus keeps surprising us though so who really knows...
With three Omicron-related recombinants getting assigned Pango lineages I'm going to write a thread covering:
- What are recombinants?
- Why are we seeing so many now?
- What exactly are the new lineages XD, XE and XF?
- How concerned should we be about them?
First off, what are recombinants?
When two related viruses infect the same cell (ie during a coinfection) the viral replication machinery can accidentally switch from one genome to the other resulting in a mixed genome - this is viral recombination.
SARS2 has been doing this all of the way through the pandemic - however its only easy to see when the two parental viruses are distantly related (for example Alpha/prevariant in the paper below) sciencedirect.com/science/articl…
Proud to have been a small part of this really important work that, I think, adds to the body of evidence that chronic infections are potential sources of SARS2 variants. Lots of evidence here but I'm going to write a short thread on one aspect I think is interesting...
One of the mutations that repeatedly, independently, arises during known chronic infections is E:T30I, after Spike: E484K, it is the most common mutation we saw in this dataset. (though worth saying it arises during *many*, but not *all* chronic infections)
However if we look at this mutation outside of these known infections its really very rare... where it is found is in sequences that look quite like chronic infections (and share many of the mutations we describe here) - nearly always singlet genomes, long branch lengths, etc
But basically the paper can be summed up here: The most common mink/ferret SARS2 adaptation attenuates the virus in humans. This probably means the risk to humans from spillback of these viruses is fairly low on a population level.