New paper mentioning ME: A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications

Countrygirl

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I am placing this paper under ME research rather than Long Covid as not only have some ME patients been proven to have mico clots (four to my knowledge) but the paper claims that it is likely relevant to ME.

https://portlandpress.com/biochemj/...central-role-for-amyloid-fibrin-microclots-in

REVIEW ARTICLE| FEBRUARY 23 2022
A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications
Douglas B. Kell

;

Gert Jacobus Laubscher;

Etheresia Pretorius



Biochem J (2022) 479 (4): 537–559.
https://doi.org/10.1042/BCJ20220016
Article history


Post-acute sequelae of COVID (PASC), usually referred to as ‘Long COVID’ (a phenotype of COVID-19), is a relatively frequent consequence of SARS-CoV-2 infection, in which symptoms such as breathlessness, fatigue, ‘brain fog’, tissue damage, inflammation, and coagulopathies (dysfunctions of the blood coagulation system) persist long after the initial infection. It bears similarities to other post-viral syndromes, and to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Many regulatory health bodies still do not recognize this syndrome as a separate disease entity, and refer to it under the broad terminology of ‘COVID’, although its demographics are quite different from those of acute COVID-19. A few years ago, we discovered that fibrinogen in blood can clot into an anomalous ‘amyloid’ form of fibrin that (like other β-rich amyloids and prions) is relatively resistant to proteolysis (fibrinolysis). The result, as is strongly manifested in platelet-poor plasma (PPP) of individuals with Long COVID, is extensive fibrin amyloid microclots that can persist, can entrap other proteins, and that may lead to the production of various autoantibodies.

These microclots are more-or-less easily measured in PPP with the stain thioflavin T and a simple fluorescence microscope. Although the symptoms of Long COVID are multifarious, we here argue that the ability of these fibrin amyloid microclots (fibrinaloids) to block up capillaries, and thus to limit the passage of red blood cells and hence O2 exchange, can actually underpin the majority of these symptoms. Consistent with this, in a preliminary report, it has been shown that suitable and closely monitored ‘triple’ anticoagulant therapy that leads to the removal of the microclots also removes the other symptoms. Fibrin amyloid microclots represent a novel and potentially important target for both the understanding and treatment of Long COVID and related disorders.
 

SWAlexander

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Thanks Countrygirl for posting.

This is in my opinion the most significant sentence:
"The result, as is strongly manifested in platelet-poor plasma (PPP) of individuals with Long COVID, is extensive fibrin amyloid microclots that can persist, can entrap other proteins, and that may lead to the production of various autoantibodies."
 

SlamDancin

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Thanks Countrygirl for posting.

This is in my opinion the most significant sentence:
"The result, as is strongly manifested in platelet-poor plasma (PPP) of individuals with Long COVID, is extensive fibrin amyloid microclots that can persist, can entrap other proteins, and that may lead to the production of various autoantibodies."
I don’t mean to take this off topic but I’ve been thinking about these autoantibodies because for me it predicts my response to medication that target the receptors with high AA levels. Specifically, trazadone and yohimbine, potent alpha1 and alpha2 adrenergic receptor antagonists give me different extremely bad reactions every time. I had AA for alpha1>alpha2 but both elevated along with M2/3. Unfortunately agonists of these receptors don’t seem to give too much benefit but I do think my reactions to antagonists show that somehow these AA’s are necessary for us to function and appear to play an agonistic role in me.
 

mitoMAN

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Howcome researchers haven’t found microclots in ME before? They seem to be kind of easy to spot? Or Maybe they just didn’t know what it was they saw.
There seem to only be a very small subset of ME/CFS patients that present microclots.
Possibly early stage after initial infection and they clear over time?
 

elvira

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There seem to only be a very small subset of ME/CFS patients that present microclots.
Possibly early stage after initial infection and they clear over time?
Too bad... but I guess if it was that easy ME would’ve been solved by now. I wonder what Pretorius will find!