Interaction of the inflammatory response and megakaryocytes in COVID-19 infection

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly across the world and has resulted in more than 4.2 million global deaths as of July 30, 2021. For reasons that remain unknown, the coronavirus disease 2019 (COVID-19) clinically manifests itself in various levels of severity, with most patients positive for COVID-19 being asymptomatic or having only mild symptoms. However, clinical studies in severely ill patients have implicated that manifestations of this infection are due in part to abnormal megakaryocyte (MK) behavior. Additionally, COVID-19–associated cytokine storms have been found to induce aberrant MK formation, primarily through interleukin-6 and Janus kinase-signal transducer and activator of transcription signaling. Autopsy reports have revealed significantly higher rates of MKs in the pulmonary and cardiac systems, which may be responsible for the high rate of thrombotic complications and abnormal coagulopathies in patients with severe forms of COVID-19. This review examines MKs and their potential function in the clinical manifestations of SARS-CoV-2 infection.