1/ This is unreal. The study title is "Same-day SARS-CoV-2 antigen test screening in an indoor mass-gathering live music event: a randomised controlled trial." It is being cited as evidence that rapid antigen tests can make social events safe. But there are a couple problems...
2/ They gave rapid tests to over 1000 people and randomly divided those who tested negative into two groups. One went to a concert, where they were encouraged to dance and sing, and the others stayed home. I encourage you to read the entire abstract in the 2 pictures below.
3/ Results: None who went to the concert tested positive for Covid eight days later, but two of those who stayed home tested positive. Yay for rapid tests, right? Not exactly.
4/ You see, when they screened study participants with rapid antigen tests before the concert, NONE tested positive. That is to say, the rapid tests had ZERO effect on the results here.
5/ One would think this would merit a mention in the abstract, but the study authors apparently didn't think so. The study title indicates it's an RCT of rapid test screening for an indoor concert, yet there's no mention in the abstract that the rapid tests were irrelevant.
6/ Perhaps even more astonishing, nowhere in the discussion section of the paper do they mention that none of the rapid antigen tests were positive and that therefore no one was screened out of participating in the concert. Instead, they sing the praises of rapid tests.
7/ The authors do not let a little thing like the total irrelevance of the rapid antigen tests to the study's results prevent them from concluding their study provides evidence of the effectiveness of rapid tests as screening tools for indoor social events. You can't make it up.
8/ Though not mentioned in the study abstract, we are eventually told that concert attendees were required to wear an N95 mask at all times, except when drinking. I'm 100% for wearing N95 masks, but this is not likely to ever be adapted as policy in the real world.
9/ The ventilation was also extraordinarily good at the concert, maintaining CO2 at or below 800 ppm, much lower than the typical school classroom.
10/ In other words, the study was designed to give a result indicating the effectiveness of rapid antigen tests, & despite its failure to provide that result, the authors manage to come to the conclusion they wanted anyway.
11/ I should add that I'm open to the possibility that rapid antigen tests could be effective in preventing Covid transmission. But this study is a joke. It's disturbing that it was published by the Lancet & is apparently being taken seriously by prominent experts.
Addendum/ This study was funded by the events company Primavera Sound Group and YoMeCorono, which I know nothing about, but which appears to be funded by dozens of (mostly) Spanish corporations. yomecorono.com/en/empresas-qu…
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Fantastic review on chronic SARS-CoV-2 infections by virological superstars Richard Neher & Alex Sigal in Nature Microbiology. I’ll do a short overview, outline a couple minor quibbles, & defend the honor of ORF9b w/some stats & 3 striking sequences from the past week.
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First, let me say that this is well-written, extremely readable, and accessible to non-experts, so you should go read the full paper yourself, if you can find a way to access it. (Just realized it’s paywalled, ugh.) 2/64nature.com/articles/s4157…
Neher & Sigal focus on the 2 most important aspects of SARS-CoV-2 persistence: its relationship to Long Covid (including increased risk of adverse health events) & its vital importance to the evolution of SARS-CoV-2 variants. I’ll focus on the evolutionary aspects.
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In SARS-2 evolution, amino acid (AA) mutations get the lion’s share of attention—& rightfully so, as noncoding & synonymous nucleotide muts—which cause no AA change‚ are mostly inconsequential. But there are many exceptions, including a possible new one I find intriguing. 1/30
I’ll discuss four categories of such “silent” mutations, two of which might be involved in the recent growth of one synonymous mutation.
Maybe the single most remarkable example of convergent evolution in SARS-CoV-2 involves noncoding mutations: the multitude of muts in major variants that have pulverized the nucleocapsid (N) Kozak sequence.
I wrote about this below & a few other 🧵s 3/
@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-…
@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 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
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
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