Coagulation abnormalities in SARS-CoV-2 infection: overexpression tissue factor
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Coagulation abnormalities in SARS-CoV-2 infection: overexpression tissue factor Zahra Eslamifar1, Mahin Behzadifard1*, Masoud Soleimani2 and Saba Behzadifard3
Abstract Among the pathways and mediators that may be dysregulated in COVID-19 infection, there are proinflammatory cytokines, lymphocyte apoptosis, and the coagulation cascade. Venous and arterial thromboembolisms also are frequent in COVID-19 patients with the increased risk of some life-threatening complications such as pulmonary embolism, myocardial infarction, and ischemic stroke. In this regard, overproduction of proinflammatory cytokines such as IL-6, IL-1β, and TNF-α induce cytokine storms, increase the risk of clot formation, platelet activation, and multiorgan failure that may eventually lead to death among these patients. Surface S protein of SARS-CoV-2 binds to its target transmembrane receptor, named as angiotensin converting enzyme 2 (ACE2(, on various cells such as lymphocyte, alveolar cells, monocytes/macrophages, and platelets. Notably, the activation of the coagulation cascade occurs through tissue factor (TF)/FVIIa-initiated hemostasis. Accordingly, TF plays the major role in the activation of coagulation system during viral infection. In viral infections, the related coagulopathy multiple factors such as inflammatory cytokines and viral specific TLRs are involved, which consequently induce TF expression aberrantly. SARS-COV-2 may directly infect monocytes/ macrophages. In addition, TF expression/release from these cells may play a critical role in the development of COVID-19 coagulopathy. In this regard, the use of TF- VIIa complex inhibitor may reduce the cytokine storm and mortality among COVID-19 patients. Keywords: Coagulopathy, SARS-CoV-2, COVID-19, Tissue factor, Thrombosis, Angiotensin converting enzyme, Angiotensin II
Introduction Although the mechanisms that activate coagulation cascade in SARS-CoV-2 infection are still unknown, they are evident to be linked to inflammatory responses [1]. inflammatory response of COVID-19 infection may be self-limited in those patients experiencing mild symptoms; however, in a smaller fraction of patients with COVID-19 infection, it is associated with the inductions of coagulopathy, disseminated intravascular coagulation (DIC) [2], cerebrovascular accidents [3], pulmonary thromboembolism, and multiorgan failure [4]. COVID19 coagulopathy was also indicated to be associated with an increase in procoagulant factors like fibrinogen as * Correspondence: [email protected] 1 Dezful university of medical sciences, Dezful, Iran Full list of author information is available at the end of the article
well as a strong increase of D-dimers that are linked with a higher mortality rate [5, 6] . Enhancement of D-dimer above 1000 ng/ml is known as a risk factor of death in COVID-19 patients [5]. Moreover, SARS-CoV-2 infected cells down-regulate the expression of ACE2 protein. As a result, the accumulation of angiotensin II (AT-II) occurs secondary to the reduced ACE2 in COVID-19 inf
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