Potential role for tissue factor in the pathogenesis of hypercoagulability associated with in COVID-19

• Published in: Journal of thrombosis and thrombolysis 2020-10, Vol.50 (3), p.479-483
• Main Authors: Bautista-Vargas, Mario, Bonilla-Abadía, Fabio, Cañas, Carlos A.
• Format: Article
• Language: English
• Subjects: Angiotensin-Converting Enzyme 2; Animals; Betacoronavirus - pathogenicity; Blood Coagulation - drug effects; Cardiology; Coronavirus Infections - blood; Coronavirus Infections - diagnosis; Coronavirus Infections - drug therapy; Coronavirus Infections - virology; COVID-19; Cytokines - metabolism; Fibrinolytic Agents - therapeutic use; Hematology; Host-Pathogen Interactions; Humans; Inflammation Mediators - metabolism; Medicine; Medicine & Public Health; Pandemics; Peptidyl-Dipeptidase A - metabolism; Pneumonia, Viral - blood; Pneumonia, Viral - diagnosis; Pneumonia, Viral - drug therapy; Pneumonia, Viral - virology; SARS-CoV-2; Thromboplastin - metabolism; Thrombosis - blood; Thrombosis - diagnosis; Thrombosis - drug therapy; Thrombosis - virology
• ISSN: 0929-5305; 1573-742X
• DOI: 10.1007/s11239-020-02172-x

In December 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 may also promote an increase in TF. TF may be a critical mediator associated with the development of thrombotic phenomena in COVID-19, and should be a target for future study.