Terrific medical article on connection between micro blood clots and long COVID
A long, complex analysis from three distinguished researchers
A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications
Abstract
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.
Conclusions
Here we have argued, and focus on the fact, that Long COVID is characterized by the presence of persistent fibrin amyloid microclots that might block capillaries and inhibit the transport of O2 to tissues, entrapping numerous inflammatory molecules, including those that prevent clot breakdown (as we have indeed recently shown)
In addition to microclot formation, significant platelet dysfunction and a systemic endotheliitis drive systemic cellular hypoxia. These pathologies can explain most, if not all, of the lingering symptoms to which individuals with long COVID refer. We have noted that amyloid microclots, platelet hyperactivation and endothelial dysfunction, might form a suitable set of foci for the clinical treatment of the symptoms of long COVID [231]. Therefore, if fibrinaloid microclots are largely responsible for the symptoms of Long COVID, their removal is to be seen as paramount for relieving these symptoms and allowing the body to repair itself.
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