potential role for tissue factor in the pathogenesis of hypercoagulability associated with in covid-19

In 2019, a new and highly contagious infectious disease emerged in wuhan, china. the etiologic agent was identified as a novel coronavirus, now known as severe acute syndrome coronavirus-2 (sars-cov-2). recent research has revealed that virus entry takes place upon the union of the virus s surface protein with the type i transmembrane metallo-carboxypeptidase, angiotensin converting enzyme 2 (ace-2) identified on epithelial cells of the host respiratory tract. virus triggers the synthesis and release of pro-inflammatory cytokines, including il-6 and tnf-α and also promotes downregulation of ace-2, which promotes a concomitant increase in levels of angiotensin ii (at-ii). both tnf-α and at-ii have been implicated in promoting overexpression of tissue factor (tf) in platelets and macrophages. additionally, the generation of antiphospholipid antibodies associated with covid-19 also promote an increase in tf. tf be a critical mediator associated with the development of thrombotic phenomena in covid-19, and should be a target for future study.