SARS-CoV-2 infection of human lung epithelial cells induces TMPRSS-mediated acute fibrin deposition

Severe COVID-associated lung injury is a major confounding factor of hospitalizations and death with no effective treatments. This study describes a non-classical fibrin clotting mechanism mediated by SARS-CoV-2 infected primary lung cells. This infection-induced fibrin formation is observed in all variants of SARS-CoV-2 infections and requires thrombin but is independent of tissue factor and other classical plasma coagulation factors. The findings reveal the inefficiency of current plasma-targeted anticoagulation therapy and suggest the need for a viral-induced ARDS animal model for treating respiratory airways with thrombin inhibitors.

Rachel Erickson, Chang Huang, Cameron Allen, Joanna Ireland, Gwynne Roth, Zhongcheng Zou, Jinghua Lu, Bernard A. P. Lafont, Nicole L. Garza, Beniah Brumbaugh, Ming Zhao, Motoshi Suzuki, Lisa Olano, Joseph Brzostowski, Elizabeth R. Fischer, Homer L. Twigg III, Reed F. Johnson, Peter D. Sun