2023 年 37 巻 1 号 p. 2-6
Coronavirus disease-2019 (COVID-19) was initially recognized as respiratory disease induced by novel corona virus (SARS-CoV-2 virus) infection. However, extremely high risks of thrombotic complications in patients with severe COVID-19 infection was noted clinically from the beginning of the COVID-19 pandemic. The virus infected into cells through their spike protein binding with angiotensin-converting enzyme 2 (ACE2). The ACE2 is expressed on both respiratory cells and vascular endothelial cells. Accordingly, it is not surprising that vascular complications such as thrombosis occur quite commonly in COVID-19 infected patients. The functionally abnormalities in endothelial cells infected by SARS-CoV-2 virus cause platelet activation and subsequent immunothrombosis. The interactions between platelets and endothelial cells are mostly determined as biorheological manner. Thus, the view from biorheological aspect is necessary to understand the mechanism of COVID-19 induced thrombosis.