Yikes! 😳
This paper has just been published. It’s a preprint so hasn’t been formally peer-reviewed, and that should be borne in mind when analysing its conclusions.
Here we report that the Spike protein from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to the blood coagulation factor fibrinogen and induces structurally abnormal blood clots with heightened proinflammatory activity. SARS-CoV-2 Spike virions enhanced fibrin-mediated microglia activation and induced fibrinogen-dependent lung pathology. COVID-19 patients had fibrin autoantibodies that persisted long after acute infection. Monoclonal antibody 5B8, targeting the cryptic inflammatory fibrin epitope, inhibited thromboinflammation. Our results reveal a procoagulant role for the SARS-CoV-2 Spike and propose fibrin-targeting interventions as a treatment for thromboinflammation in COVID-19.
Persistent life-threatening thrombotic events are a hallmark of COVID-19. Aberrant clots form in multiple organs causing significant morbidity and mortality in COVID-19 patients (1, 2). The high incidence of clotting complications has been attributed to disease severity, inflammation…
View original post 1,088 more words
CraigM350 