Thread by @beowulf888

52-1/ COVID update for epidemiological weeks 51-52 of 2024.

Here we go again! National SARS2 wastewater numbers are climbing quickly, especially in the NE and Midwest.

52-2/ Of the big 3 respiratory viruses (per CDC), COVID still trails RSV and influenza in test positivity, but has now passed RSV in the number of ED visits.

52-3/ COVID deaths are probably still falling but hospitalizations (based on incomplete data) are rising. And a rise in deaths will follow as hospitalizations rise.

52-4/ But COVID dropped to 14th place as a cause of death this year. Let's not kid ourselves, though. COVID will likely hang around on the CDC's top 15 list for the foreseeable future.

52-5/ Also, if you're unlucky enough to be hospitalized for COVID, you're more likely to die than if your were hospitalized with the flu. A Veteran's Affairs study found that 5.7% of COVID patients died within 30 days of admission, compared to 4.24% of influenza patients.

52-6/ I call your attention to 2 interesting graphs that @Truth_in_Number posted. We might be getting a wee bit better at treating severe COVID, but the rates of deaths to hospitalizations haven't changed much in 33 months. He also created a great timeline graph of COVID deaths.

52-7/ In my week 49-50 update, I conclude that the uptick in US COVID numbers is limited to certain hotspots. Well, those hotspots are spreading. SoCal sewarsheds two weeks ago vs this week...

52-8/ In NY State, COVID is still clustered around the Buffalo area and the NYC metro area + Long Island. But a few more rural counties are showing some COVID activity in their wastewater.

52-9/ XEC seems to be driving the new wave. I admit that I didn't see that coming. Its growth rate was pretty flat as of two weeks ago, but last week, XEC* jumped to 60%. I suspect sampling error (and CoV-Spectrum puts its likely avg at ~38%).

52-10/ CDC shows XEC at ~45%. When in doubt I like to look at @RajlabN's NYITCOM frequency charts. I don't see any variant other than XEC that could be pushing this wave.

It's worth noting—LP.8.1 has a high growth rate, but CoV-Spectrum shows it only running ~6% right now.

@RajlabN 52-11/ I'm going to sign off for tonight. I'll have some A(H5) slides and commentary tomorrow evening. Cheers!

@RajlabN 52-12/ There's a fascinating article in Science asking why an A(H5) pandemic hasn't started yet. Basically, no one is sure what makes some strains highly pathogenic—nor why mutations that enable human-to-human transmissibility haven't happened yet.

science.org/content/articl…

@RajlabN 52-13/ Along with some other commentators, I was under the misapprehension that Genotype D1.1 (which infects birds) was more pathogenic than B3.13 (which infects cattle). After all, all the infected dairy workers had mild symptoms, but 2 people who caught D1.1 were hospitalized.

@RajlabN 52-14/ But Tom Peacock (@PeacockFlu) set me straight. There were a cluster of D1.1 infections in Washington that weren't hospitalized. That begs the question of why some people infected with D1.1 get seriously ill, and others don't.

@RajlabN @PeacockFlu 52-15/ Don't confuse transmissibility with pathogenicity. Yes, a pandemic requires that a virus be highly transmissible, but if symptoms are mild as the infected dairy workers (i.e., conjunctivitis, sniffles, mild fever), an A(H5) pandemic would be a minor public health concern.

@RajlabN @PeacockFlu 52-16/ Much research is focused on the efficiency of Hemagglutinin (HA) and Neuraminidase (NA) proteins. HA binds to the sialic acid receptors. NA helps the virus release newly-formed viral particles from infected cells. But HA and NA have to work in a balance (see Peacock quote)

@RajlabN @PeacockFlu 52-17/ Researchers worry that improved HA and/or NA proteins will make A(H5) more transmissible and infectious. A valid concern—but what causes serious illness? From frozen corpses in AK, we have samples of the virus that caused the 1918-19 flu pandemic...
tinyurl.com/5n8369u5

@RajlabN @PeacockFlu 52-18/ The A(H1N1) influenza virus that caused the 1918-19 pandemic (killing an est. 40 million people) had a couple of characteristics that made it deadly. The PB1 protein, in particular, was associated with the expression of a viral protein called PB-F2.
tinyurl.com/5xe9752b

@RajlabN @PeacockFlu 52-19/ PB1-F2 (produced from an alternative reading frame) messed with cells' mitochondria and induced apoptosis (cell death) in immune cells like macrophages, weakening the host's immune defenses.
tinyurl.com/6cwr9b8x

@RajlabN @PeacockFlu 52-20/ Likewise, the NS1 protein in the 1918 A(H1N1) virus was highly efficient at suppressing the innate immune response—which allowed the virus to replicate unchecked in the early stages of infection.

nature.com/articles/natur…

52-21/ We'll have to see if these or some other mechanisms could make A(H5) both transmissible and pathogenic. OTOH, it could all turn into a big nothing-burger for humans. But I think it's VERY stupid of the USDoA to allow A(H5) to percolate and mutate in our food supply.

52-22/ In the worst case scenario, I'm sure Dr. Bhatty and Brainworm will have our backs! #snarkasm

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