Ryan Hisner Profile picture
Jan 23, 2022 16 tweets 7 min read Read on X
No one seems to know what BA.2 means for the world. I'm not aware of any studies on it, but I hope they come out soon. It seems apparent BA.2 will become dominant everywhere before long—as it already has in Denmark.

🧵 of graphs comparing BA.1 & BA.2 in various countries
1/16
Of all the countries with decent genetic surveillance, Denmark has the highest proportion of BA.2. 2/16
According to the Outbreak numbers compiled using @GISAID data, January 12 was when BA.2 surpassed 50% of all cases in Denmark, with 480/955 cases. 3/16
A similar conclusion was reached by @JosetteSchoenma, who's assiduously tracked BA.2 prevalence in Denmark (and elsewhere) and was pointing out its significance before anyone else. 4/16
The fact that Denmark has the highest level of Covid cases per 100,000 of any country in the world and the highest percentage of BA.2 of any country with decent sequencing data is probably not a coincidence. 5/16
The UK BA.2 numbers are far lower than in Denmark at the moment but are clearly on an exponentially increasing trajectory. It's only a matter of time before BA.2 becomes dominant there. 6/16
According to @OliasDave, BA.2 is doubling every 4 days (as a percentage of all cases) in the UK, meaning it could become dominant there in about three weeks. 7/16
Genetic surveillance outside of Denmark & the UK is far less comprehensive. The graphs therefore noisier & the trends less consistent. Still exponential increase in the proportion of BA.2 seems universal. Sweden and Norway are in the 10-15% range & exhibit similar trends. 8/16
Belgium and the Netherlands are both around 5% BA.2 with exponential increases underway. 9/16
Germany's data is pretty sparse after January 7, but there are hints of an early exponential increase in BA.2 there. 10/16
Finally, there have only been 47 sequences of BA.2 detected in the US, 17 of them in Arizona. But there can hardly be any doubt we'll see large increases in BA.2 prevalence throughout the US in the coming weeks. 11/16
Some have claimed that BA.2 is no different than BA.1 and nothing to worry about. It could turn out that way, but it seems far from certain. BA.2 has 70 mutations significantly more than the 53 of BA.1. 12/16
BA.1 and BA.2 share a set of mutations, but their mutations differ a great deal as well, both spike and non-spike. outbreak.info/compare-lineag… 13/16
One Denmark report said there was "no evidence" of increased severity from BA.2. This may turn out to be right, but it reminds me of the early declarations that there was "no evidence" Alpha or Delta were more severe. Evidence takes time to accumulate. 14/16
We can hope BA.2 won't seriously change things for the worse, but to assume it is nothing to worry about seems extremely unwise. Similar assumptions have not worked out well for us in this pandemic.

Interesting tidbit from @bicidiario here. 15/16
See this great thread by @PeacockFlu for more info on BA.2. 16/16

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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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