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.
There's been some speculation about why, despite persistent immune activation, germinal center activity, & overall elevated Ab levels, LC patients here had very low anti-spike Ab titers. I want to highlight one interesting speculative hypothesis & offer another possibility. 1/10
The ever-fertile mind of @Nucleocapsoid proffers the possibility that exosomes could be responsible for viral spread in some tissue reservoirs. I don't know much about this topic and so don't have much to say at the moment, but I'm trying to l learn. 2/
I'll offer one other possibility: the deep lung environment (or some other tissue reservoir) favors either an extreme RBD-up or extreme RBD-down conformation.
Background: The receptor-binding domain (RBD) of the spike trimer can be up or down. It has to be up to bind ACE2... 3/
A fascinating new preprint w/one very unexpected finding suggests, I believe, that a large proportion of Long Covid may be due to chronic infection in a particular bodily niche, which could be crucial for finding effective LC treatments. It requires some explaining. 🧵 1/33
First, a brief summary of the relevant parts of the preprint. They examined 30 people (from NIH RECOVER cohort) for 6 months after they had Covid, taking detailed blood immunological markers at 3 time points. 20 had Long Covid (PASC), 10 did not (CONV). 2/ biorxiv.org/content/10.110…
The PASC group showed signs of persistent, pro-inflammatory immune activation over the 6-month time period that suggested ongoing mucosal immune responses, including elevated levels of mucosa-associated invariant T cells (MAIT). 3/
Wow, BA.3.2 hits its 4th continent with a new sequence from Western Australia.
Reminder: BA.3.2 is a saltation variant resulting from a ~3-year chronic infection. It is very different from and more immune-evasive than all other current variants. 1/4
It was collected July 15, & is most closely related to the recent S African seqs from May & June.
It has an NSP5 mutation known to be beneficial (ORF1a:K3353R) & 2 new NSP12 mutations, which is unusual. Its 9 synonymous mutations indicate it has been circulating somewhere. 2/4
Seems clear now that BA.3.2 is not going away anytime soon. Its overall impact so far has been negligible, but at first BA.2.86's was as well. Once it got S:L455S (becoming JN.1) the dam burst & it set off a new wave in the global North. The question now is.... 3/4
BA.3.2 update: another sequence from the Netherlands, June 18 collection.
It belongs on the same branch as the GBW travel seq (tree gets confused by ORF7-8 deletion). Also, there are 3 artifactual muts in the GBW sequence (as usual), so the branch is shorter than it looks.
Bottom line, in my view: BA.3.2 has spread internationally & is likely growing, but very slowly. If nothing changes, its advantage vs circulating lineages, which seem stuck in an evolutionary rut, will likely gradually grow as immunity to dominant variants solidifies... 2/9
So far, this seems like a slow-motion version of what we saw with BA.2.86, which spread internationally & grew very slowly for months. But then it got S:L455S & exploded, wiping out all competitors. Will something similar happen with BA.3.2? I think there's a good chance... 3/9
Quick BA.3.2 update. Another BA.3.2.2 (S:K356T+S:A575S branch) from South Africa via pneumonia surveillance.
This means that 40% of SARS-CoV-2 sequences from SA collected since April 1 (2/5) and 50% collected after May 1 (1/2) are BA.3.2. Its foothold seems strong there. 1/3
2 interesting aspects of the new BA.3.2: 1. ORF1b:R1315C (NSP13_R392C)—This mut is in all Omicron *except* BA.3. So this may well be adaptive.
2. S:Q183H—First known antigenic spike mut seen in BA.3.2, not a major one, but one we've seen before—eg, LB.1/JN.1.9.2.1 2/3
I think the unusually long branches in the BA.3.2 tree indicate 2 things: 1. Slow growth globally—fast growth results in many identical sequences, if surveillance is sufficient
2. Undersampling—BA.3.2 most common in poorer world regions with little sequencing of late. 3/3