Immune-Mediated Coagulopathy in COVID-19 Infection.

Abstract

Viral infections, such as Epstein–Barr virus, Coxsackieviruses, and cytomegalovirus, are frequently blamed as a trigger for immune-mediated inflammation and autoimmunity, including the development of antiphospholipid syndrome. A variety of underlying mechanisms have been suggested, including virus direct overstimulatory effect on both innate and adaptive immune responses, cross-reactivity with self-antigens, and, lastly, direct effect on regulatory functions.[1] However, the high infectivity and damaging effect of coronavirus disease 2019 (COVID-19) on the respiratory tract, endothelial cells, and both innate and adaptive immunity are far beyond those of the vast majority of other viruses. While most patients with COVID-19 infection experience only mild fever, cough, myalgia, and weakness, within a few days some develop bilateral interstitial pneumonia and later acute respiratory distress syndrome, with many of them requiring long-lasting mechanical ventilation and intensive care.[2] The severity of respiratory failure and mortality in COVID-19-infected patients was reported to correlate with higher infectious dose followed by active and prolonged viral replication in pneumocytes, macrophages, and other immune cells. COVID-19 infection is characterized by a high incidence of thrombotic coagulopathies, up to the development of disseminated intravascular damage in some critical cases.[3] [4] However, the link between enhanced immune responses, endothelial damage, and coagulopathy in COVID-19-infected patients is yet to be clearly defined.