Sokhal Preeti, Singh Kinjal, Roy Riya, Sinha Saumya, Mehra Simran, Ravi Kumar Y S, Bhattacharyya Sankar, Verma Bhupendra
Department of Biotechnology, All India Institute of Medical Sciences, New Delhi, India.
Department of Biotechnology, M. S. Ramaiah, Institute of Technology, Bengaluru, India.
Rev Med Virol. 2025 Jul;35(4):e70050. doi: 10.1002/rmv.70050.
Megakaryopoiesis is a complex biological process through which haematopoietic stem cells differentiate into megakaryocyte, leading to the formation of platelets. This process is characterised by a unique differentiation pathway involving endomitosis, resulting in the polyploidisation of megakaryocyte nuclei. Megakaryopoiesis is controlled by various factors, including transcription factors, cytokines and hormones. Defects in this complex process can cause significant complications. A major issue associated with this is thrombocytopaenia, a condition characterised by abnormally low platelet counts. Thrombocytopaenia is often seen in certain cancer-related complications, genetic bone marrow disorders, autoimmune diseases, and particularly in many types of infectious diseases. Among these, dengue virus infection presents a major challenge due to its strong association with thrombocytopaenia, which greatly complicates disease management and outcomes. By integrating knowledge of megakaryopoiesis, thrombocytopaenia, and dengue infection, this review aims to provide a comprehensive understanding of megakaryopoiesis dysregulation, the molecular mechanisms of thrombocytopaenia in DENV pathogenesis and to identify potential areas for future research and clinical intervention. Additionally, this review highlights emerging insights into the role of non-coding RNAs in thrombocytopaenia and offers a better understanding of the mechanisms by which the dengue virus interferes with megakaryocyte function and platelet production, elucidating the intricate viral-host interactions that exacerbate platelet depletion.
巨核细胞生成是一个复杂的生物学过程，造血干细胞通过该过程分化为巨核细胞，进而形成血小板。这一过程的特点是存在一条独特的涉及核内有丝分裂的分化途径，导致巨核细胞核的多倍体化。巨核细胞生成受多种因素控制，包括转录因子、细胞因子和激素。这一复杂过程中的缺陷可导致严重并发症。与此相关的一个主要问题是血小板减少症，其特征是血小板计数异常低。血小板减少症常见于某些癌症相关并发症、遗传性骨髓疾病、自身免疫性疾病，尤其是在多种传染病中。其中，登革病毒感染带来了重大挑战，因为它与血小板减少症密切相关，这极大地使疾病管理和预后复杂化。通过整合巨核细胞生成、血小板减少症和登革热感染的知识，本综述旨在全面了解巨核细胞生成失调、登革病毒发病机制中血小板减少症的分子机制，并确定未来研究和临床干预的潜在领域。此外，本综述强调了对非编码RNA在血小板减少症中的作用的新见解，并更好地理解了登革病毒干扰巨核细胞功能和血小板生成的机制，阐明了加剧血小板消耗的复杂病毒-宿主相互作用。
