细胞自噬促进柯萨奇病毒B3复制的研究

Autophagy Supports Coxsackievirus B3 Replication

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.