Perspectives on Platelet Heterogeneity and Host Immune Response in Coronavirus Disease 2019 (COVID-19).

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and coronavirus disease 2019 (COVID-19) represent a global pandemic with largely uncharacterized but dire public health consequences. COVID-19 is now increasingly recognized as a thromboinflammatory disease, where thrombotic coagulopathy and intravascular coagulation are closely linked to mortality and clinical outcomes.[1] [2] [3] [4] As thrombocytopenia, systemic microvascular thrombosis, and elevated D-dimer levels reflect COVID-19 severity,[1] [2] [3] [4] cellular effectors of hemostasis and thrombosis—especially platelets—likely participate in COVID-19 pathogenesis. However, specific roles for platelets in COVID-19 as disease drivers, biomarkers, and therapeutic targets remain unspecified. Here, we highlight how platelets may be affected by COVID-19 in a manner supporting pathology, which offers insights into COVID-19 susceptibility, progression, and resolution. Like other viral infections and inflammatory states, COVID-19 likely involves alterations in platelet number, form, and function, or “platelet heterogeneity.”[5] [6] Knowledge gained over the past decade detailing mechanisms of platelet heterogeneity in inflammation and immune responses may help to gain ground in the battle against COVID-19. In turn, a surge of collaborative studies around COVID-19 pathogenesis may result in unique insights into platelet function critical to understanding and managing other inflammatory disease states.