<b>Purpose</b> <p>This review provides a brief overview of how viruses influence megakaryocyte development, maturation, and immune responses. Understanding this crucial host-virus pathophysiology will help to mitigate adverse effects by enabling the discovery of new targeted therapeutics.</p> <b>Methods</b> <p>This review examines the recent literature on virus-megakaryopoiesis interactions in the context of clinical observations, case studies, systematic cellular and molecular mechanistic data, and finally emerging therapeutic interventions to tackle virus-induced thrombocytopenia. </p> <b>Results</b> <p>Megakaryocytes are exploited by many viruses for their survival and replication, thereby impairing proliferation, differentiation, maturation, and platelet release. Such disruptions lead to immune-mediated suppression and thrombocytopenia. Viruses also induce cell death pathways at different stages of megakaryopoiesis via both receptor-dependent and independent mechanisms. Thus, viral infection has a multifaceted effect on megakaryopoiesis, with consequences for host immune regulation and disease pathogenesis. </p> <b>Conclusion</b> <p>In this review, we provide a brief overview of how viruses influence megakaryocyte development, maturation, and immune responses. Understanding this crucial host-virus pathophysiology is fundamental for developing targeted therapeutics to limit virus-induced adverse effects.</p>

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Viral subversion of megakaryopoiesis: reshaping the landscapes of immune regulation

  • J. M. Ananthu Chandran,
  • A. P. Athira,
  • Ravi Prakash Arya,
  • Anismrita Lahon

摘要

Purpose

This review provides a brief overview of how viruses influence megakaryocyte development, maturation, and immune responses. Understanding this crucial host-virus pathophysiology will help to mitigate adverse effects by enabling the discovery of new targeted therapeutics.

Methods

This review examines the recent literature on virus-megakaryopoiesis interactions in the context of clinical observations, case studies, systematic cellular and molecular mechanistic data, and finally emerging therapeutic interventions to tackle virus-induced thrombocytopenia.

Results

Megakaryocytes are exploited by many viruses for their survival and replication, thereby impairing proliferation, differentiation, maturation, and platelet release. Such disruptions lead to immune-mediated suppression and thrombocytopenia. Viruses also induce cell death pathways at different stages of megakaryopoiesis via both receptor-dependent and independent mechanisms. Thus, viral infection has a multifaceted effect on megakaryopoiesis, with consequences for host immune regulation and disease pathogenesis.

Conclusion

In this review, we provide a brief overview of how viruses influence megakaryocyte development, maturation, and immune responses. Understanding this crucial host-virus pathophysiology is fundamental for developing targeted therapeutics to limit virus-induced adverse effects.