Semin Thromb Hemost 2020; 46(07): 838-840
DOI: 10.1055/s-0040-1714272
Commentary

Immune-Mediated Coagulopathy in COVID-19 Infection

Zahava Vadasz
1  Proteomic and Clinical Flow Cytometry Unit, Bnai-Zion Medical Center, Haifa, Israel
2  Ruth and Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel
,
Benjamin Brenner
2  Ruth and Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel
3  Department of Hematology, Rambam Health Care Campus, Haifa, Israel
4  Department of Obstetrics and Gynaecology, I.M. Sechenov First Moscow State Medical University, Moscow, Russia
,
Elias Toubi
1  Proteomic and Clinical Flow Cytometry Unit, Bnai-Zion Medical Center, Haifa, Israel
2  Ruth and Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel
› Author Affiliations

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.



Publication History

Publication Date:
02 September 2020 (online)

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