Just don't get it. Why is a 2-week lag between cases and hospitalizations so hard for some people (MDs no less) to understand? We've only been studying that every day for the last 15 months.
To be specific: Israel wave lagging UK wave by ~2 weeks. Too early for champagne.
The original image (chart labels were cropped away in the above screenshots). I mean I've got the bubbly chilling like everyone else, but I don't see anything to celebrate here.
Yeah, cases triple May 24 to June 14. Hospitalizations triple June 7 to June 28. "It's different this time."
Sure, the non-vaccinated may be younger and healthier, but there will be hospitalizations and not everyone is going to regain their former levels of function.
Israel reached a minimum in case #'s about 14d ago. We can expect hospitalizations to start going up but very very slowly because cases are just now reaching ~100s per day. Expect about 1% hospitalization rate (half young unvaxxed, half older vaxxed)
By contrast, UK was at a minimum in cases 6 weeks ago, and then saw tens of thousands of cases. So we've had 4 weeks to observe the resulting hundreds of new hospitalizations, which are clearly seen above. Perhaps lower hospitalization rate than before, but it's not nothing.
Yet today we get this article: "Delta is not driving a hospitalization surge in England." What did we just see above? The writer may not consider 100s of hospitalizations as a surge, but it's irresponsible and wrong to imply that Delta is not a threat nytimes.com/2021/07/01/hea…
Actually if you look closely at the UK curves, an increase in daily cases by 5000 led to an increase in hospital admissions by 500. So that's a full 10% of cases, which is just as bad as ever. I wonder if there is severe undercounting of cases going on.
Correction about Israel: I'd expect 3% hospitalization rate (derived from 1% in the young unvaxxed and 5% in the old vaxxed, and assuming 50/50 split of cases between them, very roughly speaking). Should not try to post when sleepy. So expect just a few hospitalizations next week
Follow-up to this old thread: I analyzed the UK data as of 7/7 in a separate thread. Sure enough there are hospitalizations, at a lower per-case rate than before, but not that much lower (2.5–3.3% of cases vs 7% in January)
And now the follow-up about Israel. Sadly, but not surprisingly, the Topol-Gandhi celebration (see thread start) was indeed premature.
Weekly hospital admissions have risen by to 67 since 6/20. Rise starts somewhere between 6/20 and 6/27
We see cases start rising on 6/15. That's entirely consistent with hospitalizations rising between 6/20 and 6/27 (lag depends on if cases recorded as infection date or diagnosed date).
Actually if you look at hospitalization trends, Israel was on its way to 0 admissions this week until Delta ruined the party. That means this week's 67 new admissions are basically all from the recent Delta wave (there are ~0 patients being admitted with pre-Delta infections)
So then we can see how many cases gave rise to these 67 admissions. Because the dips lag by 5 days, we'll sum up cases from the week ending 5 days before the last weekly admission number (7/4), which is 6/24 to 6/30. That number is 1552. So hospitalization rate is 67/1552 = 4.3%
I had predicted 3% which was just a wild guess. In the Jan 2021 peak, there were 2000 hospital admissions in 1 week vs 58000 cases, or 3.4%. So the recent 4.3% rate is not lower than pre-Delta.
The 4.3% rate is not different enough from 3.4% to really analyze, but if you wanted to, you could wonder if it's because Delta is more severe (Scotland said you're 2x more likely to land in the hospital) or if people more likely to have severe disease are being diagnosed better.
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@ScienceTM This paper tells the origin story of nirmatrelvir and ML2006a4 (they are brothers) and reveals why these two drugs work so well.
It also explains the chemical basis for ML2006a4's superior activity, which goes back to a deliberate decision we made back in 2000.
The story began in March 2020 when, entering COVID shutdown, I asked if the hepatitis C virus protease inhibitor boceprevir (BPV, an oral pill) could be adapted for COVID (the viruses are distantly related).
Manually docking BPV into SARSCoV protease suggested yes (Fig. 1A).
So much for viruses evolving to less pathogenicity.
As I've said before, we might expect viruses to become more transmissible, e.g. by replicating faster or suppressing immunity. That's not less pathogenic.
A new report shows recent variants suppress innate immunity more.
There are a lot of plots, but the general gist is that BA.4/5 infection in cells generates less IFN and other innate immunity cytokines than earlier BA.1/2, and BA.4/5 shows less gain from innate immunity suppression by a drug (ruxolinitib) (because it suppressed it already)
Long-time followers recall I had postulated that SARSCoV2 was milder for children was because their innate immunity was better at suppressing viral replication until antibodies were generated.
Actually a person who could have sparked COVID19, accidentally or not, has been ID'ed in the open for a long time.
The name is Zhou Yusen. Evidence? 1. He filed a patent for SARS2 vax in 2/2020, when others only knew of SARS2 from 1/2020 2. He died from a rooftop fall in 5/2020
Those facts are not disputed, but somehow not widely discussed.
The theory isn't mine. It is described in detail by former Assistant Secretary for Preparedness and Response at the US Department of Health, Dr Robert Kadlec, above and more recently below
IgG3 antibodies bind Fc receptors on phagocytic cells like macrophages so that viral particles bound to them will be ingested and destroyed. This antibody-dependent phagocytosis (ADP) is a crucial part of the immune response to viruses...
because just one bound IgG3 molecule on a virion lead to its destruction, whereas multiple bound IgG molecules would be needed to block entry (due to multiple S proteins per virion). Also you need to clear circulating viruses to stop spread; killing infected cells is too slow.
The full DEFUSE proposal on gain-of-function experiments on bat coronaviruses is available, and I'd say it's quite shocking. It does not lay out a plan to create SARSCoV2, but does propose to identify and culture natural sarbecoviruses with the ability to infect human cells. A 🧵
There are threads interpreting the DEFUSE proposal as intending on making SARSCoV2. A careful read shows that is not the case. However the intention was to identify natural viruses with features that would help them infect cells. So it may be not much of a difference functionally
The draft proposal and related documents can be downloaded at the link below. We know DARPA rejected the final submitted proposal for being too risky. This draft proposal certainly matches that description. Were the experiments attempted? We don't know.
In 2023 about 70,000 Americans died of SARSCoV2, although >95% have some immunity. That's about 2x the usual annual deaths attributed to flu.
In people with immunity, SARSCoV2 has an infection fatality rate similar to flu, but it's much more contagious and widespread.
We spent years of effort trying to eke out small decreases in flu fatality. COVID19 has undone that and more, with >1M deaths in 3 years and now a higher hospitalization and fatality burden than flu.
Widespread annual boosting is more important for reducing death for SARSCoV2 than flu, because of its high contagiousness.
Unfortunately SARS2 booster uptake is even lower than flu or RSV.