Platelet-neutrophil interaction in COVID-19 and vaccine-induced thrombotic thrombocytopenia
Johannes Hirsch1,2, Günalp Uzun1,2, Jan Zlamal1,2
1Institute of Clinical and Experimental Transfusion Medicine, University Hospital of Tuebingen, Tuebingen, Germany.
Insights
This review explores the complex interactions between platelets and neutrophils in COVID-19-associated coagulopathy (CAC) and vaccine-induced thrombotic thrombocytopenia (VITT). Understanding this interplay is crucial for managing these thrombotic disorders.
Area of Science:
- Hematology
- Immunology
- Virology
Background:
- COVID-19 commonly causes thrombotic diathesis, known as COVID-19-associated coagulopathy (CAC).
- CAC pathophysiology involves hyperactivated platelets and neutrophil extracellular traps (NETs).
- Vaccine-induced thrombotic thrombocytopenia (VITT) is a rare, severe autoimmune disorder linked to adenoviral vector vaccines.
Purpose of the Study:
- To summarize current knowledge on platelet-neutrophil interactions in COVID-19.
- To review the role of platelet-neutrophil interplay in VITT pathophysiology.
- To highlight the importance of understanding these interactions for patient management and VITT prevention.
Main Methods:
- Literature review of existing studies on COVID-19 coagulopathy.
- Analysis of research on VITT and its autoimmune mechanisms.
- Synthesis of findings on platelet-neutrophil crosstalk in thrombotic events.
Main Results:
- Platelet and neutrophil activation are key contributors to COVID-19-associated coagulopathy.
- The bidirectional relationship between platelets and neutrophils in CAC requires further investigation.
- Understanding VITT thrombophilia is evolving, with potential implications for treatment.
Conclusions:
- Platelet-neutrophil interactions are central to the thrombotic complications of both COVID-19 and VITT.
- Further research into this crosstalk may reveal novel therapeutic targets.
- Improved understanding can aid in managing patients with these serious conditions.
Abstract:
Coronavirus disease 2019 (COVID-19) is known to commonly induce a thrombotic diathesis, particularly in severely affected individuals. So far, this COVID-19-associated coagulopathy (CAC) has been partially explained by hyperactivated platelets as well as by the prothrombotic effects of neutrophil extracellular traps (NETs) released from neutrophils. However, precise insight into the bidirectional relationship between platelets and neutrophils in the pathophysiology of CAC still lags behind. Vaccine-induced thrombotic thrombocytopenia (VITT) is a rare autoimmune disorder caused by auto-antibody formation in response to immunization with adenoviral vector vaccines. VITT is associated with life-threatening thromboembolic events and thus, high fatality rates. Our concept of the thrombophilia observed in VITT is relatively new, hence a better understanding could help in the management of such patients with the potential to also prevent VITT. In this review we aim to summarize the current knowledge on platelet-neutrophil interplay in COVID-19 and VITT.
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