肠道病毒71型致神经元病变的机制研究进展  

Advances in the Study of the Mechanism of Enterovirus 71-induced Pathological Changes in Neurons

作　　者：陈天扬 刘正芸 王欢 CHEN Tianyang;LIU Zhengyun;WANG Huan(Key Laboratory of Infectious Diseases and Biosafety of Colleges in Guizhou Province,Zunyi 563000,China;Department of Microbiology,Zunyi Medical University,Zunyi 563000,China)

机构地区：[1]遵义医科大学贵州省普通高等学校传染病与生物安全特色重点实验室,遵义563000 [2]遵义医科大学微生物学教研室,遵义563000

出　　处：《病毒学报》2022年第1期212-218,共7页Chinese Journal of Virology

基　　金：国家自然科学基金项目(项目号:81960372),题目:Drp1介导的线粒体动力学失衡在EV71致中枢神经病变中的作用机制研究;贵州省遵义市科技计划项目(项目号:遵市科合社字[2018]34号),题目:线粒体分裂调控在受EV71感染的神经肌肉细胞中的作用机制研究。

摘　　要：中枢神经系统感染是由病原体侵犯中枢神经系统引起的一类具有较高的发病率和死亡率的疾病。病毒是引起中枢神经系统感染的重要病原体之一,其中肠道病毒71型在继发神经系统症状的重症手足口病患儿中较为常见。EV71致神经元病变是其感染中枢神经系统的基础,阐明肠道病毒71型致神经元病变的机制,不仅可以促进基础病毒学研究,也能为抗病毒药物的开发提供思路,对临床肠道病毒71型致中枢神经系统感染的治疗提供支持。本文主要从肠道病毒71型侵入神经元的受体途径、损伤神经元的线粒体途径、诱导凋亡与自噬、感染胶质细胞后对神经元的旁观者效应、免疫病理机制以及病毒自身因素等多个方面,对肠道病毒71型致神经元病变机制展开综述。Central nervous system infection,caused by pathogens invading the central nervous system,is associated with high morbidity and mortality.Viruses are important pathogens that cause central nervous system infections.Of which,enterovirus 71 is more common in children with severe hand,foot and mouth disease complicating with neurological symptoms.Enterovirus 71-induced neuronopathy is the basis of the central nervous system infection.Elucidating the mechanisms of enterovirus 71-induced pathological changes in neurons not only promotes basic virological research,but also provides insight into the development of antiviral drugs,and provides support for the treatment of enterovirus 71-induced central nervous system infections.This review focuses on the mechanisms of enterovirus 71-induced pathological changes in neurons in terms of the receptor pathway for viral invasion into neurons,mitochondrial pathway that damage neurons,virus-induced apoptosis and autophagy,bystander effects on neurons after viral infection of glial cells,immunopathological mechanisms,and viral factors.

关 键 词：肠道病毒71型 神经元 致病机制 

分 类 号：R373.2[医药卫生—病原生物学]