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Mechanisms of immunothrombosis in COVID-19

Irina Portier1, Robert A Campbell1,2, Frederik Denorme1

  • 1University of Utah Molecular Medicine Program.

Current Opinion in Hematology
|July 7, 2021
PubMed

Insights

Coronavirus disease 2019 (COVID-19) causes a prothrombotic state through altered coagulation and immune cell function. This review details COVID-19's pathophysiological characteristics contributing to immunothrombosis and coagulopathy.

Area of Science:

  • Cardiovascular Science
  • Infectious Disease
  • Hematology

Background:

  • Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, presents a global health challenge.
  • While often mild, COVID-19 can induce a prothrombotic state in a significant patient subset.
  • This prothrombotic state arises from complex interactions between coagulation and immune cell functions.

Purpose of the Study:

  • To elucidate the pathophysiological mechanisms driving immunothrombosis in COVID-19.
  • To review the specific characteristics of COVID-19 that lead to a prothrombotic state.

Main Methods:

  • This is a review article, synthesizing existing research on COVID-19 and immunothrombosis.
  • The review focuses on the interplay of endothelial dysfunction, coagulation factors, and immune responses.

Main Results:

  • COVID-19 induces endotheliopathy, increasing von Willebrand factor and platelet adhesion.
  • Dysregulation of anticoagulant proteins and soluble coagulation markers (e.g., PAI-1, tissue factor) contributes to coagulopathy.
  • Platelet hyperreactivity, formation of platelet-immune cell aggregates, and neutrophil extracellular traps exacerbate thrombotic complications.

Conclusions:

  • Immunothrombosis is a critical component in the pathophysiology of COVID-19.
  • Understanding these mechanisms is essential for developing targeted therapies for COVID-19-induced coagulopathy.
Abstract

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