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

duncan said:
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I do similarly. So odd. I can only assume you only assume as to why.

Sorry to diverge from thread topic. When your teeth fracture and crumble you are more inclined to flaunt protocol.
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i am sorry, i do not understand your second and third sentences.

my only concerns about evusheld are wehther they are anything like scig or ivig in which case they could be dangerous for me. also it is not commonly used like vaccines so not much data, and no reports from pwme.

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Immunoglobulins seem to be a promising treatment for many of
my health issues, so I tried SCIG, starting at a low initial
dose (0.5mg-0.75mg) to be conservative. (This is nothing
like normal doses, much less autoimmune doses.)

SCIG at this dose caused headaches for unusually long
period, causing us to stop it. possibly weeks.

The headaches were top of head or whole head. Head movement
did not change their intensity. Once at maximum intensity,
their intensity was totally constant and never increased. I
call them "vice-like" as if head in a vice.

My doctor stopped the SCIG at that tiny dose. she thought aseptic meningitis, but i didn't have other symptoms i think.
 
interval between first and second shots seems to vary. some sources say 3w for pfizer 4w for moderna while others seem to say 8w for moderna unless exceptions.
 
Snow Leopard said:
If you are going to be getting ongoing boosters, 3/4 weeks is best for the second shot -extending the germinal centre kinetics and leading to increased diversity of antibodies.
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interesting. for clarity, sounds like you are saying, given this mrna nomenclature:

- shot 1
- shot 2 [this is apparently called "fully vaccinated" in the usa at least]
- booster 1..n [further shots after shots 1 and 2]

that shot 2 should be 3-4 weeks after shot 1, IF intending ongoing boosters, but if no plan for ongoing boosters then possibly 8w.?

but i probably will not know whether i will do boosters in advance. depends on reactions to shots and any evusheld answers/avail.
 
Samuel said:
that shot 2 should be 3-4 weeks after shot 1, IF intending ongoing boosters, but if no plan for ongoing boosters then possibly 8w.?
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Taking the 2nd shot at 8-12 weeks leads to higher short term antibody titre, because it mostly acts like a booster (expansion of existing immunity), rather than a continuation of the initial exposure.

The more neutralising antibodies you have, the more antigens that will be cleared out by the immune system, rather than used in germinal centres to train B-cells for greater diversity. This is partly why there is a delay in production in antibodies upon naive exposure, compared to subsequent exposures - producing too many 2nd rate antibodies too soon would interfere with developing highly neutralising antibodies.

But if you are going to be boosted with a 3rd shot at 3 months anyway I'd suggest the shorter interval for greater protection over time.
 
There was a paper on Covid toes published a few weeks ago, by Iwasaki, but can't find it. It only looked for biomarkers in the blood. Here is a single case study but it found what was basically expected: thrombotic vasculopathy. Biopsies are a serious limitation but medicine really has to accept that the blood does not hold all the answers. It's as if it's too convenient, almost like searching under the streetlamp because that's where the light is.


Histopathology of Persistent Long COVID Toe: A Case Report
https://onlinelibrary.wiley.com/doi/10.1111/cup.14240

During the 2020 coronavirus (SARS-CoV-2) pandemic, several cutaneous lesions were identified, including: pseudo-chilblain, vesicular, urticarial, maculopapular, and livedo/necrosis. A 59-year-old obese man with probable COVID-19 developed painful cyanosis with histopathologic capillary thrombosis of toes, and the cyanosis persisted for nearly 22 months. Shortly after initial exposure to family members with documented SARS-CoV-2, he developed upper respiratory symptoms, yet his anti-SARS-CoV-2 antibody and nasal swab RT-PCR tests were repeatedly negative. Two family members were hospitalized and one of them succumbed with documented SARS-CoV-2 pneumonia within ten days of exposure. Biopsy of the distal toe 16 weeks after initial exposure demonstrated papillary dermal capillary thrombosis with endothelial swelling, telangiectasia, and peri-eccrine lymphocytic infiltrates resembling pernio. Overall, this is the first case of biopsy of “long COVID toe” following presumed SARS-Cov-2 exposure, with demonstration of thrombotic vasculopathy, toe cyanosis, and pernio-like pathology.​

Pernio here is the medical term for chilblains. As someone who lives in an area with cold winters, I assure you that walking barefoot on cold floors cannot cause this. It was a bad idea to include this speculatively, some newspapers ran with it in the headline, FFS.
 
I've got an update on all those new Covid-19 symptoms which have just magically appeared, but can't find the "symptoms" thread. Can anyone help, please? The search didn't seem to bring it up.
 
Wits_End said:
Since those of us in England are about to lose (probably have already lost, in effect, because I get the impression that there's probably not an LFT to be had - and the other nations are only weeks behind us) access to free lateral flow tests, this article suggesting when might be the best time to use your dwindling supply of them might be of help:

When should lateral flow tests be used in England now they must be paid for?
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Interestingly, I've just been online to register the result of my negative test. You know, that registration that the government is so keen that we do after every test so they can keep track of how the disease is progressing? Well, the wording seems to have changed over the past few days: apparently the government is no longer interested in results of LFTs if they have been supplied by private companies - seemingly only those done on the free LFTs are of any interest. That'll really help them keep track. Go figure.
 
Danny Altmann on long COVID
https://www.theguardian.com/commentisfree/2022/apr/16/vaccines-long-covid-science

From article
This is now a highly infectious, upper-respiratory virus able to reinfect repeatedly – an outcome that wasn’t expected early in the pandemic. If we renege on mitigations as each round of infection draws more of all ages into chronic disability, this may be the blunder that we rue for decades to come. Even after the original wave of lockdowns and deaths has become a distantly remembered nightmare
 
Danny Altman said:
This is now a highly infectious, upper-respiratory virus able to reinfect repeatedly – an outcome that wasn’t expected early in the pandemic
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Well this isn't true. Most didn't expect it, even though they clearly should have, making this a clear failure of expertise. Some did, mostly based on other coronaviruses, as this seems to be a feature of the family. But especially so, the strategy of maximum infections is guaranteed to lead to variants, so even if it could be true with proper mitigation, the return to normal at all costs guarantees failure.

And given how many people don't have any respiratory symptoms, it doesn't make much sense to keep referring to it as a respiratory virus. It's the primary point of access but it's not like it has to comply and only enter this way. With many experiencing only GI symptoms, it likely entered their body from the GI tract.

I really expect better of experts. This whole "I didn't expect therefore no one could have known" shtick is really old and tired, especially given some of the alarms were quite explicit (and documented) about how much herd immunity was a pipe dream all along. Telling the truth really is a radical act.
 
rvallee said:
Interesting thread on thrombosis, how platelets working with neutrophils make an important part of the innate immune system, how more likely it is that there is a source for those microthromboses and microclots, which would make treatment like IVIG and apheresis unlikely to succeed (and would be a disaster anyway, as it would be impossible to make those treatments available at the scale they are needed, a similar problem that the PACE model faced even if it worked, but that didn't bother them since they knew it would never be deployed this way).

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Has persistent thrombosis even been shown in LongCOVID patients 1+ years after infection? There seems to be a lot of assumptions being made in that Twitter thread.

Some studies have shown the persistence of viral fragments in the gut several months after infection, but this is not the same as demonstrating an active infection.

Secondly, it is surprising to me to learn that apparently some medical doctors do not know that the purpose of thromboses is compartmentalisation and this is driven by the formation of immune complexes.
 
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