Department of Avian Disease, College of Veterinary Medicine, Northwest A&F University, Yangling, China.
Department of Preventive Medicine and Public Health, Faculty of Veterinary Science, University of Nyala, Nyala, Sudan.
Front Cell Infect Microbiol. 2018 Sep 3;8:304. doi: 10.3389/fcimb.2018.00304. eCollection 2018.
Newcastle disease virus (NDV) has been classified by the World Organization for Animal Health (OIE) as a notable disease-causing virus, and this virus has the ability to infect a wide range of birds. V protein is a non-structural protein of NDV. V protein has been reported to inhibit cell apoptosis (Park et al., 2003a) and promote viral replication (Huang et al., 2003), however, the mechanisms of action of V protein have not been elucidated. In the present study, a yeast two-hybrid screen was performed, and V protein was found to interact with the CacyBP/SIP protein. The results of co-immunoprecipitation and immuno-colocalization assays confirmed the interaction between V protein and CacyBP/SIP. The results of quantitative-PCR and viral plaque assays showed that overexpression of CacyBP/SIP inhibited viral replication in DF-1 cells. Overexpression of CacyBP/SIP in DF-1 cells induced caspase3-dependent apoptosis. The effect of knocking down CacyBP/SIP by siRNA was the opposite of that observed upon overexpression. Moreover, it is known that NDV induces cell apoptosis via multiple caspase-dependent pathways. Furthermore, V protein inhibited cell apoptosis and downregulated CacyBP/SIP expression in DF-1 cells. Taken together, the findings of the current study indicate that V protein interacts with CacyBP/SIP, thereby regulating cell apoptosis and viral replication.
新城疫病毒（NDV）已被世界动物卫生组织（OIE）列为重要致病性病毒，该病毒能够感染多种鸟类。V 蛋白是 NDV 的一种非结构蛋白。据报道，V 蛋白能够抑制细胞凋亡（Park 等人，2003a）和促进病毒复制（Huang 等人，2003），但 V 蛋白的作用机制尚未阐明。本研究通过酵母双杂交筛选发现，V 蛋白与 CacyBP/SIP 蛋白相互作用。共免疫沉淀和免疫共定位实验的结果证实了 V 蛋白与 CacyBP/SIP 之间的相互作用。定量 PCR 和病毒斑减少试验的结果表明，CacyBP/SIP 的过表达抑制了 DF-1 细胞中的病毒复制。CacyBP/SIP 在 DF-1 细胞中的过表达诱导了 caspase3 依赖性凋亡。用 siRNA 敲低 CacyBP/SIP 的效果与过表达时观察到的效果相反。此外，已知 NDV 通过多种 caspase 依赖性途径诱导细胞凋亡。此外，V 蛋白抑制 DF-1 细胞中的细胞凋亡并下调 CacyBP/SIP 的表达。综上所述，本研究结果表明，V 蛋白与 CacyBP/SIP 相互作用，从而调节细胞凋亡和病毒复制。
