The roles of platelets in COVID-19-associated coagulopathy and vaccine-induced immune thrombotic thrombocytopenia.

Journal Article (Journal Article;Review)

In coronavirus disease 2019 (COVID-19), multiple thromboinflammatory events contribute to the pathophysiology, including coagulation system activation, suppressed fibrinolysis, vascular endothelial cell injury, and prothrombotic alterations in immune cells such as macrophages and neutrophils. Although thrombocytopenia is not an initial presentation as an infectious coagulopathy, recent studies have demonstrated the vital role of platelets in COVID-19-associated coagulopathy SARS-CoV-2 and its spike protein have been known to directly or indirectly promote release of prothrombotic and inflammatory mediators that lead to COVID-19-associated coagulopathy. Although clinical features of vaccine-induced immune thrombotic thrombocytopenia include uncommon locations of thrombosis, including cerebral venous sinus, we speculate coronavirus spike-protein-initiated prothrombotic pathways are involved in the pathogenesis of vaccine-induced immune thrombotic thrombocytopenia, as current evidence suggests that the spike protein is the promotor and other cofactors such as perturbed immune response and inflammatory reaction enhance the production of anti-platelet factor 4 antibody.

Full Text

Duke Authors

Cited Authors

  • Iba, T; Levy, JH

Published Date

  • January 2022

Published In

Volume / Issue

  • 32 / 1

Start / End Page

  • 1 - 9

PubMed ID

  • 34455073

Pubmed Central ID

  • PMC8390120

Electronic International Standard Serial Number (EISSN)

  • 1873-2615

Digital Object Identifier (DOI)

  • 10.1016/j.tcm.2021.08.012


  • eng

Conference Location

  • United States