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Ryan Hisner Profile picture
@LongDesertTrain
Aug 21, 2022 • 10 tweets • 4 min read • Read on X
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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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More from @LongDesertTrain

Ryan Hisner Profile picture
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
Ryan Hisner Profile picture
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
Ryan Hisner Profile picture
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
Ryan Hisner Profile picture
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
Ryan Hisner Profile picture
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
Ryan Hisner Profile picture
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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