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

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...

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Bibliographic Details
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
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Summary: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.
ISSN:0929-5305
1573-742X
DOI:10.1007/s11239-020-02172-x