Platelets and SARS-CoV-2 During COVID-19: Immunity, Thrombosis, and Beyond

COVID-19 is characterized by dysregulated thrombosis and coagulation that can increase mortality in patients. Platelets are fast responders to pathogen presence, alerting the surrounding immune cells and contributing to thrombosis and intravascular coagulation. The SARS-CoV-2 genome has been found in platelets from patients with COVID-19, and its coverage varies according to the method of detection, suggesting direct interaction of the virus with these cells. Antibodies against Spike and Nucleocapsid have confirmed this platelet-viral interaction. This review discusses the immune, prothrombotic, and procoagulant characteristics of platelets observed in patients with COVID-19. We outline the direct and indirect interaction of platelets with SARS-CoV-2, the contribution of the virus to programmed cell death pathway activation in platelets and the consequent extracellular vesicle release. We discuss platelet activation and immunothrombosis in patients with COVID-19, the effect of Spike on platelets, and possible activation of platelets by classical platelet activation triggers as well as contribution of platelets to complement activation. As COVID-19-mediated thrombosis and coagulation are still not well understood in vivo, we discuss available murine models and mouse adaptable strains.

Automated summary

COVID-19 is characterized by dysregulated thrombosis and coagulation, which can increase mortality. Platelets have been found to have direct interaction with the SARS-CoV-2 virus, alerting immune cells and contributing to thrombosis and coagulation. This review discusses the immune, prothrombotic, and procoagulant characteristics of platelets in COVID-19 patients, as well as the interaction of platelets with the virus and its effects on programmed cell death and extracellular vesicle release. Murine models and mouse adaptable strains are also discussed to understand COVID-19-mediated thrombosis and coagulation.