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Updated: Nov 22, 2025

Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
COVID-19, immunothrombosis and venous thromboembolism: biological mechanisms
Joan Loo1, Daniella A Spittle2, Michael Newnham3
1College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
Insights
COVID-19 frequently causes venous thromboemboli (VTE) and microvascular issues due to inflammation and coagulopathy. Understanding immunothrombosis mechanisms is key to developing treatments for these thrombotic events.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Immunology
Background:
- COVID-19 is linked to a high incidence of thrombotic events, primarily venous thromboemboli (VTE).
- Disease severity correlates with VTE occurrence and poorer clinical outcomes.
- Microvascular abnormalities, including endothelial inflammation and microthrombi, are characteristic of severe COVID-19.
Purpose of the Study:
- To review the pathobiological mechanisms underlying immunothrombosis and VTE in COVID-19.
- To explore the intricate interplay between the hemostatic and immune systems in COVID-19-associated thrombosis.
- To identify potential therapeutic targets for managing thrombotic complications.
Main Methods:
- Comprehensive literature review of state-of-the-art research on COVID-19 and thrombosis.
- Analysis of pathobiological mechanisms including coagulopathy, endothelial dysfunction, and immune system activation.
- Examination of genetic associations and other contributing thrombotic factors.
Main Results:
- COVID-19 features a distinct coagulopathy, elevated cytokines, and activation of platelets, endothelium, and complement.
- A proinflammatory state can lead to dysregulated immunothrombosis, primarily affecting the microvasculature.
- Multifactorial processes involving intricate links between hemostatic and immune systems contribute to VTE and immunothrombosis.
Conclusions:
- Understanding the complex interplay of COVID-19-associated coagulopathy, endothelial dysfunction, and immune responses is crucial.
- This knowledge is essential for developing and evaluating novel treatments for VTE and immunothrombosis.
- Targeting these pathobiological mechanisms may improve clinical outcomes for patients with COVID-19.
Abstract:
Thrombotic events that frequently occur in COVID-19 are predominantly venous thromboemboli (VTE) and are associated with increasing disease severity and worse clinical outcomes. Distinctive microvascular abnormalities in COVID-19 include endothelial inflammation, disruption of intercellular junctions and microthrombi formation. A distinct COVID-19-associated coagulopathy along with increased cytokines and activation of platelets, endothelium and complement occur in COVID-19, which is more frequent with worsening disease severity. This proinflammatory milieu may result in immunothrombosis, a host defence mechanism that can become dysregulated, leading to excess formation of immunologically mediated thrombi which predominantly affect the microvasculature. The haemostatic and immune systems are intricately linked, and multifactorial processes are likely to contribute to VTE and immunothrombosis in COVID-19. This state-of-the-art review will explore the pathobiological mechanisms of immunothrombosis and VTE in COVID-19 focusing on: COVID-19-associated coagulopathy, pathology, endothelial dysfunction and haemostasis, the immune system and thrombosis, genetic associations and additional thrombotic mechanisms. An understanding of the complex interplay between these processes is necessary for developing and assessing how new treatments affect VTE and immunothrombosis in COVID-19.
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