细胞自噬促进柯萨奇病毒B3复制的研究  

Autophagy Supports Coxsackievirus B3 Replication

作　　者：罗小暖[1] 宋娟[1] 宋芹芹[1] 夏冬 史冰田 刘宓[1] 夏志强 王晓乐 秘春景 韩俊[1] LUO Xiaonuan;SONG Juan;SONG Qinqin;XIA Dong;SHI Bingtian;LIU Mi;XIA Zhiqiang;WANG Xiaole;MI Chunjing;HAN Jun(Chinese Center for Disease Control and Prevention,National Institute for Viral Disease Control and Prevention Beijing 102206,China)

机构地区：[1]中国疾病预防控制中心病毒病预防控制所,北京102206

出　　处：《病毒学报》2019年第1期1-5,共5页Chinese Journal of Virology

基　　金：国家传染病控制重大专项(项目号:2018ZX10102001);题目:突发急性传染病诊断试剂参考品及评价技术研究;国家传染病控制重大专项(项目号:2018ZX10734404);题目:重要传染病病原标准化鉴定关键技术研究和参比库建立;国家传染病控制重大专项(项目号:2018ZX10711001);题目:病毒感染高通量快速检测与应急筛检技术研究;传染病预防控制国家重点实验室建设项目计划(项目号:2011SKLID104);题目:肠道病毒EV71引起先天性免疫损伤机制研究~~

摘　　要：本研究探索柯萨奇病毒B3(Coxsackievirus B3,CVB3)感染引起的自噬与病毒复制之间的关系。CVB3感染HeLa细胞,并在病毒感染后6 h、8 h和10 h时检测LC3-Ⅰ蛋白、LC3-Ⅱ蛋白和p62蛋白的表达水平。结果显示CVB3病毒感染促使LC3-Ⅱ/LC3-Ⅰ比值升高,同时降低p62蛋白的表达。分别将自噬诱导剂雷帕霉素(Rapamy-cin)、自噬抑制剂3-甲基腺嘌呤(3-Methyladenine,3MA)或溶酶体抑制剂阿洛司他丁(Aloxistatin,E46D)预处理HeLa细胞2 h,CVB3感染药物处理细胞并在病毒感染6 h后收集细胞、检测CVB3病毒VP1蛋白的表达。结果显示雷帕霉素和E64D促使CVB3病毒VP1蛋白表达增加,而3MA降低CVB3病毒VP1蛋白的表达。本研究得出结论 CVB3病毒感染诱导自噬进而促进病毒复制。To explore the relationship between autophagy and viral replication in HeLa cells infected with coxsackievirus B3(CVB3),the expression levels of LC3-Ⅰ,LC-Ⅱand p62 were detected at 6 hrs,8 hrs and 10 hrs post-infection.We found that CVB3 infection increased the ratio of LC3-Ⅱ/LC3-Ⅰand decreased the expression of p62 protein.After HeLa cells were exposed to autophagy inducer Rapamycin,autophagy inhibitor 3-Methyl-adenine(3MA)or lysosomal inhibitor Aloxistatin(E64D)for 2 hrs,respectively,HeLa cells were infected with CVB3,then the expression of CVB3 VP1 was detected at 6 hrs post-infection.The results showed that both Rapamycin treatment and E 64D treatment increased the expression of VP1 protein in the HeLa cells infected with CVB3,while 3MA treatment decreased the expression of VP1 protein.CVB3 infection activated autophagy to facilitate viral replication.

关 键 词：柯萨奇病毒B3(CVB3) 自噬 病毒复制 

分 类 号：R392.2[医药卫生—免疫学] R551[医药卫生—基础医学]