"Accumulating evidence indicates that COVID-19 predisposes patients to thromboembolic disorders, but a direct association between SARS-CoV-2 and platelet dysregulation has not been reported. In this study, we demonstrated that (1) COVID-19 patients experience increased in vivo platelet activation, as evidenced by increased αIIbβ3 activation and P-selectin expression, and detectable virus RNA in the blood is associated with platelet hyperactivity; (2) platelets robustly express ACE2 and TMPRSS2; (3) SARS-CoV-2 and its Spike protein promote platelet function and thrombus formation via the MAPK pathway downstream of ACE2; and (4) recombinant human ACE2 protein and anti-Spike monoclonal antibody treatment may block SARS-CoV-2-induced platelet activation and thrombus formation. Collectively, these data suggest that SARS-CoV-2-activated platelets may result in the pro-thrombotic state described in COVID-19 patients."
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