Zou Hong, Niu Zheng, Cheng Peng, Wu Chunxia, Li Wenjie, Luo Gan, Huang Shilei
Chongqing Three Gouges Vocational College, College of Animal Science & Technology, Wanzhou, China.
College of Veterinary Medicine, Northwest A & F University, Yangling, China.
Vet Med Sci. 2025 Jan;11(1):e70182. doi: 10.1002/vms3.70182.
Peste des petits ruminants virus (PPRV), a single-stranded negative-sense RNA virus with an envelope, belongs to the Morbillivirus in the Paramyxoviridae family and is prevalent worldwide. PPRV infection causes fever, stomatitis, diarrhoea, pneumonia, abortion and other symptoms in small ruminants, with a high mortality rate that poses a significant threat to the sustainability and productivity of the small ruminant livestock sector. The PPRV virus particles have a diameter of approximately 400-500 nm and are composed of six structural proteins: nucleocapsid protein (N), phosphoprotein (P), envelope matrix protein (M), fusion protein (F), haemagglutinin protein (H) and large protein (L). Each protein has a distinct role in the virus's life cycle. Although the life cycle activities of PPRV have been widely reported, they are still limited. Research has demonstrated that PPRV has distinct adhesion factors on various cell surfaces, such as the epithelial cell adhesion factor nectin-4 or the lymphocyte adhesion factor SLAM. After attaching to the cell, the F and H proteins on the PPRV membrane interact with each other, resulting in a conformational change in the F protein. This change allows the F protein to enter the cell through direct fusion with the host cell membrane. The virus enters the host cell via the outer vesicle endocytosis strategy and replicates and proliferates through the role of caveolin, actin, dynein and cholesterol on the host cell membrane. This review summarises the viral structure, attachment mechanism and transmembrane internalisation mechanism of PPRV. The aim of this review is to provide theoretical support for the development of PPRV inhibitors and the prevention and control of PPR.
小反刍兽疫病毒（PPRV）是一种具有包膜的单链负义RNA病毒，属于副粘病毒科麻疹病毒属，在全球范围内流行。PPRV感染会导致小反刍动物出现发热、口腔炎、腹泻、肺炎、流产等症状，死亡率很高，对小反刍动物畜牧业的可持续性和生产力构成重大威胁。PPRV病毒粒子直径约为400-500纳米，由六种结构蛋白组成：核衣壳蛋白（N）、磷蛋白（P）、包膜基质蛋白（M）、融合蛋白（F）、血凝素蛋白（H）和大蛋白（L）。每种蛋白在病毒的生命周期中都有独特的作用。虽然PPRV的生命周期活动已有广泛报道，但仍很有限。研究表明，PPRV在各种细胞表面有不同的粘附因子，如上皮细胞粘附因子nectin-4或淋巴细胞粘附因子SLAM。附着到细胞后，PPRV膜上的F蛋白和H蛋白相互作用，导致F蛋白构象改变。这种变化使F蛋白通过与宿主细胞膜直接融合进入细胞。病毒通过外囊泡内吞策略进入宿主细胞，并通过宿主细胞膜上的小窝蛋白、肌动蛋白、动力蛋白和胆固醇的作用进行复制和增殖。本综述总结了PPRV的病毒结构、附着机制和跨膜内化机制。本综述的目的是为PPRV抑制剂的开发以及PPR的预防和控制提供理论支持。
