Coagulopathy, endothelial dysfunction, thrombotic microangiopathy and complement activation: potential role of complement system inhibition in COVID-19

Coronavirus disease-2019 (COVID-19) is a rapidly evolving health crisis caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is a novel disease entity and we are in a learning phase with regards to the pathogenesis, disease manifestations, and therapeutics. In addition to the primary lung injury, many patients especially the ones with moderate to severe COVID-19 display evidence of endothelial damage, complement activation, which leads to a pro-coagulable state. While there are still missing links in our understanding, the interplay of endothelium, complement system activation, and immune response to the SARS-CoV-2 virus is a surprisingly major factor in COVID-19 pathogenesis. One could envision COVID-19 becoming a novel hematological syndrome. This review is to discuss the available literature with regards to the involvement of the complement system, and coagulation cascade and their interaction with endothelium.

Automated summary

COVID-19, caused by SARS-CoV-2, is a rapidly evolving health crisis characterized by primary lung injury, evidence of endothelial damage, complement activation, and heightened coagulability. The interplay of endothelium, complement system activation, and immune response to the virus plays a major role in COVID-19 pathogenesis, potentially leading to the development of a novel hematological syndrome. This review aims to discuss the involvement of the complement system, coagulation cascade, and their interaction with endothelium in COVID-19.