鉴定VP1与GM130的相互作用，这可能与柯萨奇病毒B3诱导的急性胰腺炎的发病机制有关。

Identification of the interaction of VP1 with GM130 which may implicate in the pathogenesis of CVB3-induced acute pancreatitis.

作者信息

Li Xiuzhen, Xia Yanhua, Huang Shengping, Liu Fadi, Ying Ying, Xu Qiufang, Liu Xin, Jin Guili, Papasian Christopher J, Chen Jack, Fu Mingui, Huang Xiaotian

机构信息

Department of Medical Microbiology, School of Medicine, Nanchang University, Nanchang, Jiangxi, China.

Department of Basic Medical Science, School of Medicine, University of Missouri Kansas City, Kansas City, MO, USA.

出版信息

Sci Rep. 2015 Aug 28;5:13324. doi: 10.1038/srep13324.

Coxsackievirus B3 (CVB3) is a causative agent of viral myocarditis, pancreatitis, and meningitis in humans. Although the susceptibility of CVB3-induced acute pancreatitis is age-dependent, the underlying mechanisms remain unclear. Here we identified the host factor Golgi matrix protein 130 (GM130) as a novel target of CVB3 during CVB3-induced acute pancreatitis. The viral protein VP1 interacted with GM130, disrupted GM130-GRASP65 complexes, and caused GM130 degradation, which may lead to disruption of the Golgi ribbon and development of acute pancreatitis in mice. Interestingly, the expression level of GM130 in mouse pancreas was age-dependent, which was nicely correlated with the age-associated susceptibility of CVB3-induced acute pancreatitis. Furthermore, interference RNA-mediated knockdown of GM130 significantly reduced CVB3 replication in HeLa cells. Taken together, the study identified GM130 as a novel target of CVB3, which may implicate in the pathogenesis of CVB3-induced acute pancreatitis.

柯萨奇病毒B3（CVB3）是人类病毒性心肌炎、胰腺炎和脑膜炎的病原体。尽管CVB3诱导的急性胰腺炎易感性存在年龄依赖性，但其潜在机制仍不清楚。在此，我们确定宿主因子高尔基体基质蛋白130（GM130）是CVB3诱导急性胰腺炎过程中CVB3的一个新靶点。病毒蛋白VP1与GM130相互作用，破坏GM130-GRASP65复合物，并导致GM130降解，这可能导致高尔基体带的破坏以及小鼠急性胰腺炎的发生。有趣的是，GM130在小鼠胰腺中的表达水平存在年龄依赖性，这与CVB3诱导急性胰腺炎的年龄相关易感性密切相关。此外，RNA干扰介导的GM130敲低显著降低了CVB3在HeLa细胞中的复制。综上所述，该研究确定GM130是CVB3的一个新靶点，这可能与CVB3诱导急性胰腺炎的发病机制有关。