@TeslaStars Demonstrably, his claims aren't true, given the overloaded hospitals all over the world. But to be more specific.
1) His first *preprint* actually says that there's 95% odds that the risk of death is "1% to 81% as high as Delta" (Delta being ~2x that of Alpha)
@TeslaStars Note that that's *unadjusted* hazard ratios (single-factor), and that the adjusted hazard ratios (which they didn't even bother trying for for mortality, given the huge CIs) trend to higher hazard ratios than the unadjusted.
@TeslaStars 2) Paxlovid is awesome, but it's also unobtanium, and will continue to be for quite some time. Pfizer hopes to make 120 million treatments (for a planet of 8 billion people) this year, but mainly in the second half. Experts are dubious: endpts.com/pfizer-says-it…
@TeslaStars Paxlovid costs over $500 per course. IF there's "only" an average of one infection per person per year, that's a good fraction of 1% of the US GDP spent just on Paxlovid. Better buy Pfizer stock.
@TeslaStars 3) You cannot just take vaccine efficacies against Delta mortality (which were similar to efficacy against hospitalization) and act like they apply to Omicron, a strain defined by its evasiveness.
We don't have mortality efficacy, but we do have hosp:
Note that combining in efficacy against infection doesn't apply when you're pursuing an "everyone gets infected" scenario.
@TeslaStars As for the IFR: IFR doubled from Alpha to Delta, and Alpha was in turn associated with a higher IFR than Wuhan-Hu-1, which was estimated at 0,7%. Our CIs on mortality from Omicron are all over the board. We can't even look to South Africa yet because deaths are still growing.
@TeslaStars (To head people off: no, you can't just compare cases to deaths, you have to do cohort studies to account for time, differences in the cohort (younger wave with Omicron, etc).
@TeslaStars You also can't factor in unobtanium Paxlovid into the equation. Tomas is also quite silent about the fact that Omicron rendered some of our best treatments, like REGN-COV2, near useless.
Lastly, the net mortality from a virus is not simply its IFR, but IFR * (R0-1).
@TeslaStars Influenza has an R0 barely over 1. Delta has an R0 of 5-9. Omicron appears to have somewhat less of an R0, but combined with a high level of immune escape. Regardless, an order of magnitude higher. Which is how it keeps overloading hospitals.
@TeslaStars Not to mention this with regards to everyone's favourite, flu comparisons:
I'll reiterate: hospitals aren't overflowing on a lark.
@TeslaStars Tomas talks a lot about building immunity. Except the fact that past immunity offers almost no protection against Omicron. You should not expect the reverse.
First off, that's at two weeks post-infection (peak nAbs), before the rapid post-infection waning period (followed by a slower long-term decline). But more to the point...
There's a logarithmic correlation - not a linear one - between neutralization and protection. That 2-week peak is enough to, say, boost a person from 50% to 80% protection. But then comes post-infection nAbs waning.
@TeslaStars Most critically, however, ***Evolution Isn't Planning To Stop For You***. Omicron already appears to have a more contagious sibling, BA.2:
The concerning aspect of BA.2 is that it appears to be *less* immune evasive, yet more contagious - i.e....
@TeslaStars ... a higher R0. In the past, where we've seen strains develop a higher R0, higher hospitalization and mortality rates have come with it.
But it's so early, we can say very little about BA.2; we're still learning about BA.1 and the clade in general.
@TeslaStars The simple fact is that people are not just developing antibodies to SARS-CoV-2 now. They've had them for ages. They're just having their past immunity bypassed.
Every infection is a net NEGATIVE on the global herd immunity register, a new change to evolve new strains.
@TeslaStars Take Manaus, for example. It was initially cited as an early example of a city that had achieved herd immunity.
Until Gamma came along and caused a far worse, deadlier wave.
@TeslaStars Okay, but surely they got herd immunity THEN, right?
Oh wait.
I'll repeat: herd immunity through infection is a myth. Infection creates strains to BYPASS herd immunity.
@TeslaStars This thread is not intended as doom-and-gloom. We've made huge progress at lowering the mortality rate, despite our evolving foe. We will continue to do so.
But misleading about the current status helps nobody. There's still a slog ahead.
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"people who were invited because they got a negative result at the time the other subjects got a positive result". It's unclear if anything was done to ascertain a lack of infection beyond this (possible question on the questionnaire?). There is no discussion of serology.
3. Most single-dose individuals were infected than vaccinated, while most two-dose individuals were vaccinated then infected. A poor showing for single-dose individuals mainly just implies that "vaccination doesn't cure Long COVID", and doesn't say much about prevention.
(a) COVID patients (community-enrolled), whether with Long COVID (LC) or not (MC), have dramatically elevated interferon levels persisting 4 months after...
..infection - something not seen in uninfected controls (UHC) or people who caught "cold" coronaviruses (HCoV). As a reminder, interferons are cytokines sound the alarm call to viral infection and form a complex regulatory network of pro- and anti-inflammatory signals. Elevated..
...levels of pro-inflammatory interferons - as observed - promote aggressive T-cell responses; symptoms can range from asymptomatic to feeling ill to serious pathological states.
(b) While in non-Long COVID patients most IFN levels have significantly declined by 8 months, in...
Summary: sniffer dogs can detect Long COVID patient sweat samples 51,1% of the time with a 0% false positive rate on controls.
Handlers are blinded to the sample locations, so not a Clever Hans effect. There's detail about how patients were sampled but not controls, though one presumes it's the same. I rather suspect unintentional scent marking distinctions, either in handling of samples...
... or in things that Long COVID patients tend to do (or not do) that the general public does not, rather than a dog-detectable odour eminating from their bodies. It's easy to accidentally mark samples with odours that humans cannot detect.
This evening, I decided to put all of my masks to a proper qualitative fit test using a nebulizer, bitrex solution, and improvised hood. From the upper left, counterclockwise:
Summary: In SARS-CoV-2 patients, there's dramatic alteration of gene expression in the olfactory bulb of the brain, yet this doesn't correlate with the virus's presence or absence...
... in the olfactory bulb. Seeking to explain this, they checked for a marker of connectivity of sensory nerve fibres (afferants) called OMP-1, and as controls looked at a marker for olfactory lesions (TH) and general. neural activity (SNAP-25)
Results?
OMP-1 - the connectivity marker - was highly depleted in COVID patients (A) with anosmia, in comparison to non-COVID patients. No difference was seen in the marker for lesions (TH) or neural activity (SNAP-25). It thus appears that the pathology is upstream of the olfactory bulb.
Hey @elonmusk, any way to rollback this horrid UI update? It's destroyed the usability of common controls on the bottom bar. Literally imposdible to have things like defrost and seat heaters as one-click. Is hiding "defrost" even legal? Shouldn't be.
Who designed this thing, and who approved it? All logic is gone. Like, if I swipe my music down off the screen, them swipe back up, it's not the music that comesup, but the giant climate control screen! Is that "intuitive" or "helpful"?
With all the things that vanished from the bottom bar, it's now mostly blank unused space, on the most important part of the screen - even if I fill the custom bar from the limited subset of choices.
What were designers thinking with moving wiper controls so far from the wheel?