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Ryan Hisner Profile picture
@LongDesertTrain
Jan 23, 2022 • 16 tweets • 7 min read • Read on X
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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

Ryan Hisner Profile picture
Nov 24
@SolidEvidence There was yet another paper this week describing someone chronically infected, with serious symptoms, but who repeatedly tested negative for everything with nasopharyngeal swabs. On bronchoalveolar lavage (BAL), they were Covid-positive. 1/ ijidonline.com/article/S1201-…Image
@SolidEvidence BAL is very rarely performed, yet there must be dozens of documented cases now where NP-swab PRC-negative patients who were very ill tested positive by BAL. This has to be way more common than we realize.

If we had a similar GI test, I imagine we'd find something similar. 2/
@SolidEvidence Importantly, the patient was treated and improved, likely clearing the virus for good. Many, maybe most, chronic infections could be treated and cleared. But they have to know they're infected for that to happen. 3/
Read 4 tweets
Ryan Hisner Profile picture
Nov 22
Superb thread here by @jbloom_lab that meshes well with what we've seen over the last few months in SARS-CoV-2 spike evolution: not much.

IMO, nothing significant has happened since the NTD-glycan-adding muts (T22N, ∆S31) & Q493E appeared. This 🧵 explains why. 1/6
Read full 🧵for explanation, but the short story is that the best apparent escape mutations all interact w/something else—like a nearby spike protomer or other important AA—making mutations there prohibitively costly.

In short, the virus has mutated itself into a corner. 2/6
It's very hard to effectively mutate out such a local fitness peak via stepwise mutation in circulation since multiple simultaneous muts might be required to reach a higher fitness peak. 3/6

Read 6 tweets
Ryan Hisner Profile picture
Nov 10
It's an interesting thought. I think the evidence is strong that all new, divergent variants have derived from chronic infections. The first wave of such variants—Alpha, Beta, Gamma—IMO involved chronic infections lasting probably ~5-7 months. It's controversial to say.... 1/15
…that Delta originated in a chronic infection, but I think the evidence that it did is strong. One characteristic of chronic-infection branches is a high rate of non-synonymous nucleotide (nuc) substitutions (subs)—i.e. ones that result in an amino acid (AA) change. 2/15 Image
For example, if 80% of nuc subs in coding regions cause an AA change, that’s a very high nonsynonymous rate. The branch leading to Delta has 17 AA changes—from just *15* nuc subs! That’s over 100%. How is this possible? 3/15
Read 15 tweets
Ryan Hisner Profile picture
Nov 3
I'd add that XEC's had no noticeable impact on cases & isn't likely to going forward barring a serious change, which we've not seen since S:Q493E & the glycan-adding S:S31-/S:T22N appeared months ago. Next major change seems likely to take the form of an entirely new variant. 1/4
I've been in lockstep with @SolidEvidence and @JPWeiland on this front. Despite the sensational early growth advantages XEC appeared to have, it never seemed likely to me ever to have a noticeable real-world impact. 2/4
In fact, XEC resembles BA.5.2 + ORF1b:T1050N, which had a similar growth advantage in summer 2022. That one, however, never had a sexy name like "XEC" that was distinct from other major contemporary variants so it passed unnoticed. Names matter. 3/4
Read 4 tweets
Ryan Hisner Profile picture
Oct 11
Molnupiravir-created mutants still show up intermittently, mostly in Australia and Japan. A remarkable one popped up today: A KP.3.1.1 with 94 private mutations. 1/6 Image
The closest related sequences are from the same region and from about 1 month earlier, suggesting these 94 consensus mutations were acquired in about one month, and possibly a shorter period of time. 2/6 Image
It has the classic MOV signature of an extremely high percentage of transversions, primarily C->T and (especially) G->A.

93/94 mutations are transitions
27/94 are C->T
38/94 are G->A

More detailed discussion of this in 2022 thread below.

3/6
Read 6 tweets
Ryan Hisner Profile picture
Oct 5
There aren't many convergent mutations in ORF1b in chronic-infection sequences. But many of the ones that do show up repeatedly are also highlighted in this study looking at NSP12 mutations that developed in immunocompromised pts treated with remdesivir. 1/4
I've spent hundreds of hours compiling a list of >3500 likely chronic-infection sequences & have created an imperfect, approximate measure for how overrepresented a mutation is in chronic sequences compared to circulating sequences (as measured by independent acquisitions). 2/4
Of the top 10 ORF1b chronic-infection-specific mutations on this list (occurring ≥5 times), five appeared in the remdesivir-treated patients in this study: Q435K, C455Y, V783I, M785I, & C790Y.

V783I was in 2 study patients & is also the most common of these in chronics. 3/4 Image
Read 5 tweets

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