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Ryan Hisner Profile picture
@LongDesertTrain
Sep 25 • 7 tweets • 3 min read • Read on X
It seems more certain than ever: getting Covid is bad for your brain.

This study, which found cognitive effects at 1 year post Covid to be equivalent to brain aging from age 50 to 70, looked only at hospitalized patients. But as Dr. Topol says.... 1/7
...another recent study—a controlled experimental one involving young (18-30), healthy volunteers—found significant negative cognitive effects from mild illness 1 year after the challenge trial.
Mild illness. Healthy 18-30-year-olds. 1 yr later. 2/7
And that study almost certainly underestimates the cognitive effects of 1 mild case of Covid. As @Mike_Honey_ pointed out, during the following year, which encompassed the Delta, BA.1, BA.2, & BA.5 waves, many in both groups were undoubtedly infected. 3/7
But the uninfected group no doubt suffered on average more infections since they did not obtain the degree of immunity the infected group did. So the negative cognitive effects are really a measure of less than 1 infection. 4/7
These studies reinforce the conclusions of the Biobank brain study, which found significant brain shrinkage for those who got Covid compared to those who didn't.
Reaction of many in public health to that study: hide results, lest we frighten people. 5/7
There are a multitude of other studies with similar findings, but I single out these because of how well designed & clearly objective the studies were: a prospective trial with matched controls; a controlled experimental challenge trial; & before-and-after brain scans. 6/7
Getting sick is bad for you, & getting Covid is almost certainly worse than any comparably common illness.

So get your vaccinations &, as much as possible, clean the air you breathe. The latter should be a top public health priority but sadly is not. 7/7

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More from @LongDesertTrain

Ryan Hisner Profile picture
Sep 21
I’ve mostly pooh-poohed the rise of XEC for 2 reasons:

#1. Its spike is almost identical to the dominant KP.3.1.1
#2. I don’t think its advantage over KP.3.1.1 is large enough to make a significant real-world impact.

But one aspect of XEC is noteworthy: The demise of N*.
1/20
I’ve talked a lot about nucleocapsid before, mostly in this 120-tweet thread that was too long for anyone to want to read. Nucleocapsid is by far the most abundant SARS-CoV-2 protein. Nothing else comes close. It is very, very important. 2/20
An essential aspect of N is its phosphorylation. Phosphorylation involves the attachment of a highly negatively charged phosphate to (usually) an S or T amino acid. We even know how it happens in the SARS-CoV-2 N. It’s pretty neat. 3/20
Read 20 tweets
Ryan Hisner Profile picture
Sep 8
Update on XEC: the weekly growth advantage of XEC relative to KP.3.1.1 has withered to approximately zero in Germany, the country XEC has been in longest and which has by far the highest proportion of XEC sequences. 1/13
Image
The country of origin is generally the best place to compare a new variant to others. But globally, most seqs have been collected outside Germany (World: ~225, Germany: ~60), & these deserve some weight.

And globally, it looks like an XEC massacre. 2/13 Image
But global growth figures are often misleading. There have been virtually no XEC detected in Asia or Australia, for example. Apart from Germany, only Denmark, the Netherlands, the UK, & Canada have >20 seqs and >0.3% prevalence in the past 2 months. So let's look at these. 3/13 Image
Read 15 tweets
Ryan Hisner Profile picture
Sep 1
Lots of talk about the XEC variant lately. It's a fast variant, but I want to emphasize two things.

First, I don't think XEC is much faster than the dominant KP.3.1.1. Germany is the only country w/enough seqs for a reliable growth estimate & it's pretty modest & uncertain. 1/6 Image
A variant w/such a small growth advantage (assuming it's accurate) takes months to grow to dominance. And such modest advantages do not result in any noticeable change in case levels, so I don't expect XEC to have any real impact. By the time it would become dominant... 2/6
...it's almost certain that some other, more dramatic evolutionary event will have taken place, whether that be another chronic-infection-derived saltation variant or simply further stepwise spike mutations on top of current variants. 3/6
Read 6 tweets
Ryan Hisner Profile picture
Jul 17
KP.3, w/the unusual Q493E mutation, now dominant globally. To me, it's the first major spike change—involving real structural/epistatic change as opposed to treadmilling, stepwise antibody-evasion mutations merely keeping pace w/population immunity—since JN.1 emerged. 1/23
Most spike mutations affect ACE2 binding similarly in BA.2, XBB.1.5, & JN.1—e.g., Y453F confers a large incr in ACE2 affinity in all—so the XBB.1.5 deep mutational scanning info from @bdadonaite & @jbloom_lab is still invaluable. But Q493E is different. 2/
In both XBB.1.5 and BA.2 spike backgrounds, Q493E imposes a devastating hit to ACE2 affinity—so large that no variant with it could survive & circulate.
Data below from:
Bloom Lab XBB.1.5 DMS -
BA.2 RBD heat map - 3/ dms-vep.org/SARS-CoV-2_XBB…
jbloomlab.github.io/SARS-CoV-2-RBD…
Image
Read 25 tweets
Ryan Hisner Profile picture
Jul 3
AI is a disaster for journalism. Here are a two examples of AI hallucinations on the FLiRT variants of JN.1, which are named after spike mutations F456L & R346T.

This one from @NewstalkFM says FLiRT stands for "F-Type Recombinant Lineage," a term invented from whole cloth. 1/3
When I Googled that name, a clear AI hallucination dutifully copied & pasted by "journalists," I accidentally stumbled on another.

This one, from the Manchester Evening News via Yahoo News, says FLiRT stands for "Fresh Lineage of Rapid Transmission." 2/3 Image
How many other things that we read from such "news organizations"—better described as transcribers of ChatGPT word vomit—are AI hallucinations?

We need publicly funded journalism, yesterday. See one proposal from @DeanBaker13 described below. 3/3 thenation.com/article/societ…
Read 4 tweets
Ryan Hisner Profile picture
Jun 29
@suprion_verlag @dfocosi @yunlong_cao @RajlabN @BenjMurrell @SystemsVirology @SimonLoriereLab @EricTopol @TRyanGregory @tylernstarr @JPWeiland @siamosolocani @CorneliusRoemer The basic pattern has been that we occasionally see huge evolutionary jumps with no intermediate sequences (BA.1, BA.2, BA.5, BJ.1/XBB, BA.2.3.20, BA.2.86, & many others), which in reality evolved stepwise within a single, chronically infected individual.
@suprion_verlag @dfocosi @yunlong_cao @RajlabN @BenjMurrell @SystemsVirology @SimonLoriereLab @EricTopol @TRyanGregory @tylernstarr @JPWeiland @siamosolocani @CorneliusRoemer Then, after such a variant begins circulating, it begins to pick up mutations, primarily in the spike protein, which evade antibodies that are widespread in the population. The specific mutations vary somewhat with each new variant, but there's a lot of common ground as well...
@suprion_verlag @dfocosi @yunlong_cao @RajlabN @BenjMurrell @SystemsVirology @SimonLoriereLab @EricTopol @TRyanGregory @tylernstarr @JPWeiland @siamosolocani @CorneliusRoemer R346T, for example, has been acquired again and again. Various mutations at E484 and F486 have been common as well, and there are many others that could be mentioned. In some cases, these mutations seem to have arrived at a quasi-endpoint (for now)—∆Y144 or F486P, for example.
Read 5 tweets

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