Ryan Hisner Profile picture
Jan 25, 2022 9 tweets 5 min read Read on X
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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More from @LongDesertTrain

Mar 26
So it's clear that BA.3.2 preferentially infects children, something we have never seen before in a SARS-CoV-2 variant.

Why?

The question's baffled me, but after a suggestion from Darren Martin, I think I have an explanation that makes sense.
1/16
I've tried to make sense of BA.3.2's penchant for kids by considering its unique spike: more compact, more closed, & more antibody-evasive than any other variant.

But I think another feature of BA.3.2 is responsible: its wholesale deletion of ORF7a, ORF7b, & ORF8 (∆ORF78).
2/
∆ORF78 is rare but not unheard of; it was in several late XBB variants (GW.5.1.1, FW.1.1, GE.1.2, etc) & a few branches of other variants. I've long thought these late XBB had an advantage in some population subsector, but I didn't suspect kids.
3/
Read 18 tweets
Mar 24
You have to wonder for how long we will continue seeing infections from 2020 continue to show up (in absurdly high quantities) in wastewater.
1/16
I suspect that the number of people continuously infected since 2020 or 2021 is much larger than we realize. It's impossible to prove, but there are case studies where a chronically infected person gets infected by a new variant, which drives out the original virus...
2/16
...which consequently leaves no trace that the person was chronically infected before the super-infecting variant—took over.

Why then are some Cryptic WW variants resistant to being outcompeted by newer variants?
3/16
Read 16 tweets
Mar 22
While the final outcome for BA.3.2 is uncertain, its unique characteristics—extensively remodeled spike NTD & SD1/SD2, novel S2 muts, & total deletion of ORF7a/7b/8—make it the best candidate for co-dominance we've seen, which could mark a new era in SARS-2 evolution. 1/
Until now, the broad pattern of SARS-2 evolution has been:

1) Emergence of a saltation variant originating in a chronic infection

2) Rapid growth/global dominance & a variant-driven wave of infection—especially if it emerges in late fall/winter (BA.1, XBB.1.5, JN.1). 2/
3) Stepwise evolution over the next few months/years, usually without driving major waves (the JN.1-descended KP.3.1.1 being a notable exception).

4) Repeat

3/
Read 34 tweets
Dec 29, 2025
Very proud to be a co-author on this comprehensive preprint on the novel, growing saltation lineage BA.3.2, together with @Tuliodna, Darren Martin, Dikeledi Kekana, and lead author @graemedor. 1/9
I would normally write a summary 🧵 of the BA.3.2 mutational analysis here, but as much of my contribution parallels my previous BA.3.2 threads I'll just link to those here, w/brief descriptions of each.

This is my first, big-picture BA.3.2 🧵. 2/9
Short thread from June when the first travel BA.3.2 sequences showed up. I think my prediction from back then has pretty much been borne out. 3/9
Read 9 tweets
Dec 24, 2025
BA.3.2 emerged in Nov 2024 after ~3 years of intrahost evolution with >50 new spike AA muts, but since then, it's changed very little. Could the drug molnupiravir (MOV) galvanize BA.3.2 into pursuing new evolutionary paths? A new 89-mut MOV BA.3.2 seq suggests it could. 1/11 Image
Background on MOV: It's a mutagenic drug. Its purpose is to cause so many mutations that the virus becomes unviable & is cleared. But we've long known this often does not happen. Instead, the virus persists in highly mutated form & can be transmitted. 2/
I was an author on a paper published in @Nature that conclusively showed not only that MOV has created highly mutated, persistent viruses, but that these viruses have transmitted numerous times. See 🧵 below by lead author @theosanderson. 3/
Read 11 tweets
Dec 22, 2025
The most valuable viral research tools—@nextstrain & CovSpectrum—are being destroyed, not only blocked from new data but now forbidden from even sharing info from the PAST. Why?

Because GISAID is run dictatorially by a con man, paranoid egomaniac, & liar named Peter Bogner. 1/
I use CovSpectrum & Nextstrain every day—& I'm not the only one. Every Covid thread I've ever posted here has relied partly on CovSpectrum & Nextstrain for information & visuals. These vital tools have now been stolen from us by a world-class grifter. 2/ thinkglobalhealth.org/article/to-fin…Image
For years scientists knew something was very, very wrong with GISAID, but the breakout story (from which much of this 🧵is based) came 2 years ago in @ScienceMagazine from @sciencecohen & Martin Enserik. 3/
science.org/content/articl…
Read 22 tweets

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