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Author Spotlight: High-Sensitivity Tissue Factor Activity Assay for Plasma Diagnosis
Published on: December 29, 2023
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Coagulation abnormalities in SARS-CoV-2 infection: overexpression tissue factor.
Zahra Eslamifar1, Mahin Behzadifard2, Masoud Soleimani3
1Dezful university of medical sciences, Dezful, Iran.
Thrombosis Journal
|December 16, 2020
Summary
COVID-19 infection dysregulates inflammation and coagulation, increasing clot risk. Targeting tissue factor (TF) may mitigate cytokine storms and reduce mortality in patients.
Area of Science:
- Infectious Diseases
- Hematology
- Immunology
Background:
- COVID-19 is associated with dysregulated inflammation, lymphocyte apoptosis, and coagulation cascade activation.
- Thromboembolism, including pulmonary embolism, myocardial infarction, and ischemic stroke, is a frequent complication.
- Proinflammatory cytokines (IL-6, IL-1β, TNF-α) contribute to cytokine storms, promoting clot formation and multiorgan failure.
Purpose of the Study:
- To investigate the role of tissue factor (TF) in COVID-19 coagulopathy.
- To explore the potential of TF pathway inhibitors in managing COVID-19 complications.
Main Methods:
- The study discusses the binding of SARS-CoV-2 S protein to ACE2 receptors on various cells.
- It highlights the activation of the coagulation cascade via the tissue factor (TF)/FVIIa pathway.
- The role of viral infections and inflammatory cytokines in aberrant TF expression is examined.
Main Results:
- SARS-CoV-2 infection can directly affect monocytes/macrophages, leading to TF expression and release.
- This TF expression is implicated in the development of COVID-19-associated coagulopathy.
- Overproduction of cytokines exacerbates clot formation and platelet activation.
Conclusions:
- Aberrant TF expression, driven by viral infection and inflammation, is central to COVID-19 coagulopathy.
- Inhibiting the TF/FVIIa complex presents a potential therapeutic strategy.
- Targeting TF may reduce cytokine storms and improve mortality rates in COVID-19 patients.
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