As Omicron has washed over the US, infecting perhaps 25% of the population already & likely to reach 40% by mid-February—see thread by @trvrb below—it has driven down almost all other respiratory pathogens, with one curious exception I’ll get to later. 1/9
This is not entirely unexpected. Viral infections trigger both innate and adaptive immune responses that can prevent infection by other viruses. Behavior changes likely contribute to this pattern as well. 2/9
There have been some claims that rhinovirus infection protects against SARS-CoV-2 infection. As you can see in the graph below, SARS-CoV-2 and RV prevalence seem almost perfectly inversely related in recent months. 3/9 news.yale.edu/2021/06/15/com…
Rhinoviruses typically peak in spring & fall & are lower during winter, when influenza, coronaviruses, HMPV, RSV, & other viruses thrive, suggesting these viruses & RVs compete & inhibit one another in some way. Great article on RVs by @MackayIM below. 4/9 virologydownunder.com/rhinovirus-ram…
One would expect more closely related viruses to compete most vigorously. The rapid displacement of one SARS-CoV-2 variant by another in this pandemic seems to confirm this. 5/9
The history of influenza also suggests closely related viruses undergo intense competition. It’s thought H3N8 dominated in late 19th c. but was replaced by H1N1 in the 1918 pandemic. H1N1 in turn was displaced by H2N2 in 1957, which vanished when H3N2 appeared in 1968. 6/9
Curiously, H3N2 has persisted through the emergence of H1N1 in 1977 (possible lab leak) & pH1N1 in 2009. The paper linked to below suggests this is because the 2 major proteins on their surfaces are quite different & antigenically distinct. 7/9 journals.asm.org/doi/10.1128/mB… 6/
This makes the one exception to the downward trend in all non-Omicron respiratory pathogens all the more remarkable. As Omicron has risen, everything else has fallen—except the seasonal coronaviruses, which have risen in step with Omicron. 8/9
OC43, NL63, and 229E have all contributed to the recent rise in seasonal coronavirus cases. (HKU1 has been absent for nearly 2 years now.) I don’t have any idea why this would happen. I’d love to hear what others’ hypotheses are though. 9/9
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@yaem98684142 @TBM4_JP This analysis is extremely flawed.
There is nothing abnormal about BA.2.86 appearing in multiple countries shortly after discovery. This has been the norm lately w/reduced surveillance. 1/
@yaem98684142 @TBM4_JP The mutational spectrum analysis is poorly done. It cites a single study looking at the mutational spectrum in *three* immunocompromised individuals. Needless to say, this sample size is WAY too small. 3/
@yaem98684142 @TBM4_JP Furthermore, the IC people examined did not give rise to highly divergent variants with a large number of spike mutations. They appear to have accumulated a very modest number of mutations, with few substitutions in spike. The sequences themselves are apparently not published. 4/
Interesting recombinant showed up today from Texas. It's a mixture of B.1.595, BA.1, and some flavor of JN.1. Most of the genome is from B.1.595. The ancestry of this one is clear: it directly descends from a B.1.595 sequence collected in January 2023, also in Texas. 1/11
When the B.1.595 was collected this infection was >1 yr old, w/no sign of Omicron. BA.1 ceased circulating ~1 year prior.
Now a BA.1 spike appears w/just 5 changes from baseline BA.1, none in the RBD—S12F, T76I, Q271K, R765H, S939F.
This is a zombie BA.1 spike. 2/
There are only a few signs of JN.1, & they're scattered. In ORF1a, we see JN.1's V3593F, P3395H, & R3821K, but the NSP6 deletion btwn these—universal in Omicron—is absent. In
M has JN.1's D3H + T30A & E19Q (in JN.1 & BA.1), yet A63T—also in both BA.1 & JN.1 is absent. 3/11
An awesome preprint on the novel, unsung SARS-CoV-2 N* protein came out recently, authored by @corcoran_lab & Rory Mulloy. I’ve previously written on N*’s demise in XEC, the top variant in late 2024/early 2025. But…
1/34
…this preprint, along with another great study by the @DavidLVBauer, @theosanderson, @PeacockFlu & others prompted me to take a closer look...
2/34biorxiv.org/content/10.110…
...and for reasons I’ll describe below, I now believe rumors of N*’s death are exaggerated.
First, XEC is in terminal decline, replaced by variants with full N* expression, so N* is back in fashion.
3/34 journals.plos.org/plosbiology/ar…
@DameSunshine @SharonBurnabyBC B.1.1.529 wasn't/isn't a real variant; it's a placeholder that represents a putative ancestor of BA.1/BA.2/BA.3.
Bad sequences and/or coinfections tend to get categorized as B.1.1.529:—they have enough Omicron muts to be ID'd as Omicron but so much dropout/mixed signals...
1/
@DameSunshine @SharonBurnabyBC ...that a specific designation isn't possible. Travel sequencing in the US is done by Ginkgo Bioworks. Their sequences are generally poor quality & they upload *pooled* sequences—against database guidelines. The B.1.1.529 here are likely low-quality/pooled sequences from GBW.
2/
@DameSunshine @SharonBurnabyBC I think it's entirely possible that a new, divergent variant will emerge this summer. There are hints with BA.3.2 & a 50-spike-mutation BQ.1.1 that has transmitted at least once. Other similar chronic infection-derived variants are undoubtedly lurking all over, unsequenced.... 3/
Incredible how quickly @yunlong_cao & co provide us w/info on the latest emerging SARS-CoV-2 variants.
Already, we have great data on BA.3.2 (the divergent saltation lineage detected in South Africa & the Netherlands & NB.1.8.1, an emerging contender for global dominance. 1/9
BA.3.2 is a clear outlier on the antigenic cartography map—as expected given the enormous differences between its spike protein & every other circulating variant. 2/9
It's unsurprising, therefore, that BA.3.2 evades antibodies from human sera more effectively than any other variant, though the degree of its superiority is striking. 3/9 biorxiv.org/content/10.110…
About 1 month after this monster BQ.1.1 appeared, an even more extreme sequence has shown up in Alberta. Like the BQ, it has 50 private spike mutations, but it also has >40 AA mutations elsewhere in the genome. 1/6
They include the full panoply of NSP3, NSP12, & N muts I've written about previously. ORF1a:S4398L is the most common mutation in the 4395-4398 region, this has ∆S4398, a rarity also seen in a few other extremely divergent seqs w/this constellation. 2/6
In a theme that's become familiar, it's added two spike NTD glycans, N30 (via F32S) and N155 (via S155N+F157S).
Another chronic-infection leitmotif (first noted by @SolidEvidence): reversions to common or consensus residues in related Bat-CoVs, including SARS-1. 3/6