Summarised by Centrist
Researchers at the University of California – San Francisco (UCSF) have identified fibrin, a blood-clotting protein, as a major factor in driving COVID and long COVID symptoms.
The study, published in Nature, revealed that fibrin binds to the spike proteins of the SARS-CoV-2 virus, forming clots that trigger inflammation and neurological issues.
Previous studies have suggested that blood clotting results from inflammation, but these results reveal it is the clotting that occurs first.
“Our study is the first to report causality for fibrin as the root of inflammation and brain pathology after COVID infection,” said Dr Katerina Akassoglou, senior author of the study.
The team tested a novel antibody designed to block fibrin, which reduced clotting and neurological symptoms in mice. A version of this antibody is currently in human clinical trials.
Other treatments, like nattokinase–a supplement made from fermented soybeans (natto)–and combinations of anticoagulants, have shown promise for addressing clotting in long COVID patients.
Additionally, sulodexide–a drug that helps prevent blood clots and treats blood vessel issues by thinning the blood and protecting the lining of blood vessels–has proven effective without raising bleeding risks.
The researchers also cite a study of over 99 million vaccinated individuals that found a slight increase in clotting diseases was observed with certain COVID vaccines.
The study also suggested that abnormal clotting may suppress cancer-fighting immune cells, which may explain the rise in post-COVID cancer cases.