Title:Fibrinogen, Fibrin, and Fibrin Degradation Products in COVID-19
Volume: 23
Issue: 17
Author(s): Kadri Kangro, Alisa S. Wolberg and Matthew J. Flick*
Affiliation:
- Department of Pathology and Laboratory Medicine, UNC Blood Research Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Keywords:
Fibrinogen, fibrin, D-dimer, coagulation, fibrinolysis, COVID-19.
Abstract: Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is the highly pathogenic
and highly transmissible human coronavirus that is the causative agent for the worldwide
COVID-19 pandemic. COVID-19 manifests predominantly as a respiratory illness with symptoms
consistent with viral pneumonia, but other organ systems (e.g., kidney, heart, brain) can also become
perturbed in COVID-19 patients. Accumulating data suggest that significant activation of the
hemostatic system is a common pathological manifestation of SARS-CoV-2 infection. The clotting
protein fibrinogen is one of the most abundant plasma proteins. Following activation of coagulation,
the central coagulation protease thrombin converts fibrinogen to fibrin monomers, which selfassemble
to form a matrix, the primary structural component of the blood clot. Severe COVID-19 is
associated with a profound perturbation of circulating fibrinogen, intra- and extravascular fibrin
deposition and persistence, and fibrin degradation. Current findings suggest high levels of fibrinogen
and the fibrin degradation product D-dimer are biomarkers of poor prognosis in COVID-19.
Moreover, emerging studies with in vitro and animal models indicate fibrin(ogen) as an active player
in COVID-19 pathogenesis. Here, we review the current literature regarding fibrin(ogen) and
COVID-19, including possible pathogenic mechanisms and treatment strategies centered on clotting
and fibrin(ogen) function.
