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Perspectives on Platelet Heterogeneity and Host Immune Response in Coronavirus Disease 2019 (COVID-19)Funding This work is supported by the National Institutes of Health (grant R01HL146549).
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.    As thrombocytopenia, systemic microvascular thrombosis, and elevated D-dimer levels reflect COVID-19 severity,    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.”  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.
Article published online:
03 September 2020
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