The biology of coronavirus COVID-19 - including research and treatments

All this stuff about thrombosis seems to me to be hot air from people who don't understand immunology. I am fairly sure it is all an artefact.

 

I think this is the study they're basing it on (from the Guardian article):
https://www.researchsquare.com/article/rs-1205453/v1
https://www.researchsquare.com/article/rs-1205453/v1.pdf?c=1640823028000

It was an uncontrolled study, a lot of details are left out, such as how long people were ill for, severity of specific symptoms etc.

I'd appreciate your input on their methodology on 'Platelet activation criteria', skip down to Tables 2-4.

 

I had never heard of assays of this type. They seem to be looking at thrombus formation ex vivo in plate-poor plasma. I have no idea what relevance that has to putative presence of clots in vivo.

 

I recently had tests ordered that seemed to have this sort of platelet assay in mind, or something similar. The tests included Thrombotic Risk Profile and Collagen Binding Assay, among others. Most seemed to pertain to clotting stuff.

My platelet counts trend low, but I believe this was an effort to see how LC issues might manifest in pwME, in particular micro clots.

 

I'm noticing lots of concern over unexplained liver and kidney damage being seen in many countries. Many likely have noticed the controversy over unexplained cases of liver failure, and the debate over whether the widely circulating virus known to cause organ damage may be at cause. But it's also kidneys.

Lungs and heart feature prominently, sure, but especially kidneys and livers. The filter organs. Filters in general tend to have problems with being clogged up, it really puts a dent in their ability to filter things.

Hey, good thing there isn't some possible explanation about some tiny, uh, clumps of stuff being common in the fluid that is being filtered, or something? In general, of course. Maybe it isn't the case for those patients.

It's just odd that those two dots aren't joined as a common hypothesis. Hey, it could be total coincidence that a pandemic virus known to cause clumps in the bloodstream is happening at the same time as some people's blood filters are mysteriously shutting down.

I'm pretty sure the full explanation has a few extra steps to this, but it's really odd that this connection is missing from the discussion. Hear many hoofbeats? Clearly a bunch of weirdos walking around with coconuts.

 

I have no idea where else to put this. Continuing on the issue of idiopathic hepatitis cases, the leading speculation is that following 2 years of reduced social contact, children were less exposed to viruses, like adenovirus, thus leaving them... more susceptible to adenovirus? I don't follow the logic but the idea seems to be that immunity from common viruses comes from constantly being exposed to them, I guess in small amounts (huge assumption but whatever), and thus not being exposed regularly leaves us weaker.

This seems to be an offshoot of the "modern world is too clean" hypothesis, nevermind that much of humanity absolutely does not live in conditions anywhere near aseptic that many espouse as one reason why we suffer so much from allergies, autoimmune diseases and so on.

Somehow, though, not much thinking of the fact that we are exposed to massively higher doses and variety of various pathogens, most of which would normally remain half-way around the world, in addition to pollution, plastics in our bloodstream, etc. Or how specific antibodies are, rendering this concept invalid given, you know... evolution!

So I have to ask... is this a thing? Does medicine believe this, and would thus explain the general indifference to common infections? Driving the idea that it's not a big deal for most people to be sick regularly since this is how we... I guess build immunity from being sick? Somehow that it doesn't achieve the goal doesn't seem to phase anyone.

Because it's hard to think of another interpretation to those bizarre ideas. They seem to be common, and on the topic of mysterious cases of hepatitis, seems to drive the explanation over the lack of regular exposure to pathogens. And boy are there smug people assuring everyone that Covid has nothing whatsoever to do with this. Which could be true, but the speculation offered instead is very flimsy.

Because this is also the real idea behind "herd immunity" with SARS-CoV-2. It's not actual immunity, that's a pipe dream, rather it's the idea that it's normal and good for people to be regularly exposed to "mild" (only in terms of healthcare utilization and typical cases anyway) pathogens because it's literally the underlying idea? And with mutations evading immunity, I've seen it asserted plainly that medical authorities are just hoping that at one point there will be a constant state of reinfections, but they will be mild so it's OK.

I can't find fault in how those two ideas are just sides of the same coin. Are we being failed because of a belief that it's good for people to be regularly sick, as way to avoid... being regularly sick?

 

It was also pointed out (by a gastroenterologist on Twitter) that we haven't seen any pathology reports from the explanted livers. Even if the path findings were non-specific, that would probably be helpful for others to have some visibility into.

Whatever is causing this childhood acute liver failure, it is important. Each transplant is a very big deal, not just for the patient and their family, but also for the health service that maintains that transplant over (hopefully very many) years and manages the inevitable illness episodes relating to acute rejection and generally medication/immunosuppression. Even if all goes as well as possible, it upends a family's circumstances.

 

The 041 adenovirus they have found in some of the children usually causes gastroenteritis. If children are meeting it later in life because of pandemic behaviours you would expect it to cause a more severe stomach disease not attack the liver.

If it has changed behaviour and is now causing a different disease that cannot be due to a delay in becoming infective it has to be a change in the genetics of the virus not the experience of the children.

Some adenoviruses do cause hepatitis but the disease they cause is different from that in these children.

 

https://twitter.com/user/status/1520283624225996801

 

The whole "the virus will become mild over time if we allow mass infections has a very strong 'this plan must work because it's the only one we have'" that are common at the end of films and TV but rarely work out in real life. And since this is real life, well...

Evolution happens to promote the organism's survival, it does not care about human affairs or a good cinematic ending.

https://twitter.com/user/status/1529965612956405761

 

https://twitter.com/user/status/1532367164161810432

 

https://www.theguardian.com/world/2...n-first-wave-get-no-immune-boost-from-omicron

 

Direct link to paper in above Guardian article:
Immune boosting by B.1.1.529 (Omicron) depends on previous SARS-CoV-2 exposure (2022, senior author Altman)

 

They are certainly hanging a lot of conclusions on blood from 4-6 people there. I wonder if there is some effect that people who were more likely to be re-infected after three doses and a past infection probably just have weaker immunity in general, so the causality might be running the other way. Not so much imprinting as people with weaker immunity before re-infection continue to have weaker immunity after re-infection.

 

Is there a possibility the liver is the key,I suspect I have partial aHUS and see common features
Is the liver damaged altered or triggered causing a complement imbalance and over reaction to viruses

Mild aHUS,low iron,low platelets and kidney haematuria and thickened blood due to complement activation

 

What is aHUS?

 

https://en.wikipedia.org/wiki/Atypical_hemolytic_uremic_syndrome

 

https://twitter.com/user/status/1543150440791031808

 

BA.2.75 sure is worrying (or could still turn out to be nothing), but calculating a relative growth advantage with a few dozen sequences over the last month and with who knows what ascertainment bias (almost all the sequences are from India, mostly from one state), isn't really going to tell us much.

 

The relative transmissibility is likely due to immune escape in vaccinated/prior infected individuals (or a biased cohort), rather than being way higher than measles.