Inverse relationship between rhinovirus & SARS-CoV-2 still holding strong. Seems clear some form of viral interference is happening here. But is the causation all one way (SARS2-->RV) or does it go both ways? As someone likely suffering an RV infection right now, I'm curious 1/10
There is some evidence that rhinovirus infection protects against Covid by activating interferon-stimulated genes (ISG). ISG are activated upon SARS-CoV-2 infection as well, but with a delay that allows the virus to replicate & establish infection. 2/10 rupress.org/jem/article-st…
Here's another 2021 study showing experimental evidence that RV impedes Covid. Remarkably, SARS-CoV-2 was inhibited even when rhinovirus was introduced 24 hours after inoculation. 3/10 academic.oup.com/jid/article/22…
By blocking the interferon response stimulated by RV infection, the experimenters proved that it was through the stimulating the innate interferon response that RV interferes with SARS-CoV-2. 4/10
At least one eminent virologist and rhinovirus specialist maintains the viral interference between SARS-CoV-2 and rhinovirus works both ways, as one would expect, even if the interferon response to Covid is somewhat weaker than that evoked by RVs. 5/10
It seems to be generally accepted that a large rhinovirus wave that accompanied the start of the school year in some European countries in 2009 delayed the onset of the H1N1 pandemic flu ("swine flu") waves there. 6/10
More recent research seems to confirm what was suspected at the time: rhinovirus infection provides protection against influenza A. 7/10
BTW, I'm not trying to make a point here, certainly not that we should seek out RV infection to prevent flu or Covid—RV is making me quite miserable right now. I want to avoid future RV infection as much as possible. I just find this all fascinating. 8/10
Viral interference happens with other viruses as well, and the original Omicron wave drove down the prevalence of almost all other respiratory viruses with one very strange exception: the seasonal coronaviruses. I still don't understand that one. 9/10
Usual caveat: I'm not an expert in these matters and have likely left out important considerations or said something stupid. Corrections & additional information from genuine experts (& others) welcome. 10/10
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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…