Ryan Hisner Profile picture
May 26, 2021 7 tweets 2 min read Read on X
1/7 Satan is trending on Twitter. I recall what Mark Twain said about him.
"I am quite sure that I have no race prejudices, and I think I have no color prejudices nor caste prejudices nor creed prejudices. Indeed, I know it..."
2/7 "I can stand any society. All that I care to know is that a man is a human being—that is enough for me; he can't be any worse."
3/7 "I have no special regard for Satan; but I can at least claim that I have no prejudice against him. It may even be that I lean a little his way, on account of his not having a fair show."
4/ "All religions issue bibles against him & say the most injurious things about him,but we never hear his side. We have none but the evidence for the prosecution, yet we have rendered the verdict. To my mind, this is irregular. It is un-English; it is un-American; it is French."
5/7 "We may not pay [Satan] reverence, for that would be indiscreet, but we can at least respect his talents."
6/7 "A person who has for untold centuries maintained the imposing position of spiritual head of four-fifths of the human race, and political head of the whole of it, must be granted the possession of executive abilities of the loftiest order."
7/7 "In [Satan's] large presence the other popes and politicians shrink to midges for the microscope. I would like to see him. I would rather see him and shake him by the tail than any other member of the European Concert."

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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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