1/6 At a private gathering of 33 Pfizer-triple-vaccinated health care workers in the Faroe Islands, 21 were infected with Omicron—a superspreading event among 3-dose-vaccinated people. All received dose #3 within 2.5 months of the event. Very discouraging. medrxiv.org/content/10.110…
2/6 All participants tested negative within 36 hours of the event: five with rapid tests and the other 28 with PCR tests. Median age was 45. Only four of the 21 infected had any comorbidities.
3/6 And very similar to the Oslo Christmas superspreader event (where 79 of 80 infected were symptomatic, with 74 having >3 symptoms), all 21 experienced symptoms. There is virtually no asymptomatic infection with Omicron it seems.
4/6 While most had mild illness, moderate and severe symptoms were not as rare as one would hope in a group of young, healthy, triple-vaccinated individuals. Thankfully, none were hospitalized.
5/6 As seen in the Oslo superspreading event and described anecdotally elsewhere, the incubation period was short: 3.24 days on average. Five of those infected still had symptoms at the time of their interview (12-14 days after infection).
6/6 CDC messaging has consistently downplayed the risk of transmission among the vaccinated, & it needs to stop. These people did everything right: they were triple-vaxxed & all tested before gathering. It didn't matter.
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
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
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
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
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
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
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
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…
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