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尼帕病毒（Nipah virus,NiV）属于副黏病毒科亨尼帕病毒属，是一种高传染性人兽共患病毒，具有跨物种传播能力强和病死率高等特点，严重威胁全球公共卫生安全。NiV可通过表面G蛋白与宿主受体Ephrin-B2/B3结合介导病毒入侵并依赖F蛋白实现膜融合；感染后可引发血管内皮损伤、合胞体形成及中枢神经系统病变。NiV还可通过P基因编码的多种蛋白（P、V、W、C蛋白）协同作用，在干扰素产生及信号传导等多个层面拮抗宿主先天免疫反应，从而实现免疫逃逸。然而，现有关于NiV的研究结果相对分散，对NiV致病过程各关键环节之间的联系仍缺乏系统梳理。本文系统综述NiV的结构特征及其致病机制，重点关注病毒入侵与复制、破坏血管内皮屏障、神经系统损伤及免疫逃逸等关键过程，为诊断治疗、抗病毒药物和疫苗研发提供理论参考。
Abstract：Nipah virus(NiV), a member of the genus Henipavirus within the family Paramyxoviridae, is a highly contagious zoonotic pathogen. Characterized by its profound capacity for interspecies transmission and a high case-fatality rate, NiV poses a severe threat to global public health. NiV can invade the host by binding its surface attachment glycoprotein(G) to host receptors ephrin-B2/B3, and realize membrane fusion facilitated by the fusion glycoprotein(F). Following infection, the virus induces vascular endothelial injury, syncytium formation, and central nervous system(CNS) lesions. Furthermore, NiV achieves immune evasion through the synergistic action of multiple proteins(P, V, W, and C) encoded by P gene, which antagonize the host innate immune response at multiple levels, including interferon(IFN) production and downstream signal transduction. However, current research findings on NiV remain relatively fragmented, lacking a systematic elucidation of the interplay among the key stages of its pathogenesis. Therefore, the structural features and molecular pathogenesis of NiV were comprehensively summarized herein, with a specific focus on crucial processes such as viral invasion and replication, disruption of the vascular endothelial barrier, neurological damage, and immune evasion. Ultimately, this aims to provide a theoretical basis for clinical diagnosis, therapeutic interventions, and the development of antiviral drugs and vaccines.
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基本信息:
中图分类号:R373
引用信息:
[1]谭湘湘,张苗苗,符峻炎,等.尼帕病毒感染的分子致病机制研究进展[J].病毒学报().
基金信息:
广东省自然科学基金面上项目(项目号:2026A1515010110),题目:靶向赤羽病毒NSs蛋白的小分子化合物ABT-199抑制其复制的分子机制; 广东青年创新人才项目(项目号:2025KQNCX081),题目:赤羽病毒Gc介导宿主BNIP3促进线粒体自噬有利于其复制的分子机制
2026-08-31
2026-08-31
2026-08-31