Hypercoagulability in COVID-19: A review of the potential mechanisms underlying clotting disorders
Author:
Open Access
- 1 January 2021
- journal article
- review article
- Published by SAGE Publications in Sage Open Medicine
- Vol. 9
Abstract
Severe acute respiratory syndrome coronavirus-2 has emerged as a new viral pandemic, causing Coronavirus disease 2019 (COVID-19) leading to a wide array of symptoms ranging from asymptomatic to severe respiratory failure. However, coagulation disorders have been found in some patients infected with SARS-CoV-2, leading to either a clotting disorder or hemorrhage. Several mechanisms attempt to explain the mechanism behind the pro-coagulant state seen with COVID-19 patients, including different receptor binding, cytokine storm, and direct viral endothelial damage. SARS-CoV-2 has also been recently found to bind to CLEC4M receptor, a receptor that participates in the clearance of von Willebrand Factor and Factor VIII. The competitive binding of SARS-CoV-2 to CLEC4M could lead to decreased clearance, and therefore a promotion of a pro-coagulative state; however, an experimental study needs to be done to prove such an association.Keywords
This publication has 61 references indexed in Scilit:
- The C-type lectin receptor CLEC4M binds, internalizes, and clears von Willebrand factor and contributes to the variation in plasma von Willebrand factor levelsBlood, 2013
- Review: Viral infections and mechanisms of thrombosis and bleedingJournal of Medical Virology, 2012
- Role of angiotensin II in plasma PAI-1 changes induced by imidapril or candesartan in hypertensive patients with metabolic syndromeHypertension Research, 2011
- Interactions between coagulation and complement—their role in inflammationSeminars in Immunopathology, 2011
- Systemic versus localized coagulation activation contributing to organ failure in critically ill patientsSeminars in Immunopathology, 2011
- The M, E, and N Structural Proteins of the Severe Acute Respiratory Syndrome Coronavirus Are Required for Efficient Assembly, Trafficking, and Release of Virus-Like ParticlesJournal of Virology, 2008
- Architecture of the SARS coronavirus prefusion spikeNature Structural & Molecular Biology, 2006
- The complement component C5a induces the expression of plasminogen activator inhibitor-1 in human macrophages via NF-κB activationJournal of Thrombosis and Haemostasis, 2006
- Cellular entry of the SARS coronavirusTrends in Microbiology, 2004
- Interleukin 6 Induces the Expression of Vascular Endothelial Growth FactorJournal of Biological Chemistry, 1996