COVID-19, immunothrombosis and venous thromboembolism: biological mechanisms

Research output: Contribution to journalArticlepeer-review

Authors

Colleges, School and Institutes

External organisations

  • College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK

Abstract

Thrombotic events that frequently occur in Coronavirus disease 2019 (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 pro-inflammatory 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 & haemostasis, the immune system & 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. Keywords: Pulmonary Embolism, Innate Immunity, Viral infection, Cytokine Biology, Respiratory Infection

Details

Original languageEnglish
JournalThorax
Early online date6 Jan 2021
Publication statusE-pub ahead of print - 6 Jan 2021