Kell, Douglas B, Pretorius, Etheresia · The Biochemical journal · 2023 · DOI
This study proposes that in Long COVID and other post-infection diseases, a blood protein called fibrinogen can fold into an abnormal shape that forms sticky clots called fibrinaloids. These unusual clots may trigger the immune system to attack the body's own tissues (autoimmunity) because the abnormal folding creates new structures the immune system doesn't recognize. The authors suggest this process is similar to what happens in prion diseases and other protein-misfolding conditions.
Understanding whether fibrinaloid microclots initiate autoimmunity could explain both the clotting abnormalities and immune dysregulation observed in ME/CFS and Long COVID. If fibrinaloid formation is indeed a primary mechanism, it could open new avenues for prevention and targeted treatment. This hypothesis bridges multiple disease mechanisms and may help unify observations across post-infection syndromes.
This review does not provide direct experimental or clinical evidence that fibrinaloids cause autoimmunity in Long COVID patients—it presents a mechanistic hypothesis. The study does not demonstrate that fibrinaloid formation is necessary and sufficient for disease, nor does it establish the relative contribution of this mechanism compared to other factors. Correlation between fibrinaloid presence and autoantibody generation in human disease remains to be firmly established.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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