内质网应激在丙肝病毒感染发病学中作用的研究进展  

Research progress on the role of endoplasmic reticulum stress in pathogenesis of hepatitis C virus infection

作　　者：李明皓 范亮亮 项荣 LI Ming-hao;FAN Liang-liang;XIANG Rong(Xiangya School of Medicine, Central South University, Changsha 410013, China)

机构地区：[1]中南大学湘雅医学院,湖南长沙410013

出　　处：《基础医学与临床》2022年第2期316-320,共5页Basic and Clinical Medicine

基　　金：国家科技重大专项(2017ZX10103005-006)。

摘　　要：丙型肝炎病毒(HCV)常扰乱内质网稳态,其复制中间产物的积累可导致内质网应激(ERS),与多种疾病的发生密切相关。为了应对内质网应激所带来的有害影响,细胞激活未折叠蛋白反应(UPR)和凋亡通路。在病毒感染的初期,未折叠蛋白反应主要用于清除病毒产生的蛋白和其他中间产物;而当感染进一步深化,稳态不能维持时细胞则激活凋亡通路。但以上通路也可被病毒蛋白操纵而深化感染并减弱抗病毒反应。The infection caused by hepatitis C virus(HCV)often disturbs the momeostasis of endoplasmic reticulum.Accumulation of replication intermediates can lead to endoplasmic reticulum stress(ERS),which is closely related to the occurrence of many diseases.In order to prevent the harmful effects of endoplasmic reticulum stress,cells activate unfolded protein response(UPR)and apoptosis pathway.In early stage of virus infection,unfolded protein reaction is a main function to remove the proteins and other intermediates produced by the virus and when the infection deepens and the homeostasis is no longer to be maintained,the cell activates the apoptosis pathway.However,these pathways can also be manipulated by viral proteins to deepen infection and inhitit antiviral mechanism.

关 键 词：内质网应激 未折叠蛋白反应 丙型肝炎病毒 凋亡 

分 类 号：R512.63[医药卫生—内科学]