EV71诱导has-miR-200b表达并促进自身复制的机制  

Enterovirus 71 induces has-miR-200b expression to promote viral replication

作　　者：胡静平 王燕 傅煜轩 HU Jingping;WANG Yan;FU Yuxuan(Institutes of Biology and Medical Sciences,Soochow University,Suzhou 215123,China;Department of Stomatology,Affiliated Suzhou Hospital of Nanjing Medical University,Suzhou Municipal Hospital,Suzhou 215001,China)

机构地区：[1]苏州大学生物医学研究院,苏州215123 [2]南京医科大学附属苏州医院/苏州市立医院,苏州215001

出　　处：《生物学杂志》2022年第5期21-25,共5页Journal of Biology

基　　金：国家自然科学基金青年科学基金项目(No.31900679);江苏高校优势学科建设工程资助项目。

摘　　要：通过高通量测序检测、荧光素酶报告基因实验以及Western Blot探究miR-200b在EV71病毒复制过程中的作用。结果表明:高通量miRNA测序发现EV71感染后宿主细胞中has-miR-200b的表达显著上升,特异性抑制miR-200b的表达能够抑制EV71病毒复制;荧光素酶报告基因实验发现,miR-200b能够直接靶向结合干扰素刺激基因IFIT5的3′-UTR区域;进一步研究证实在EV71病毒感染过程中所诱导的miR-200b的表达增加能够抑制IFIT5表达进而抑制Ⅰ型干扰素应答。研究表明,EV71病毒感染能够诱导宿主细胞内miR-200b表达增加,进而抑制干扰素刺激基因IFIT5的表达,导致胞内干扰素应答抑制,从而有利EV71病毒复制。The role of miR-200 b in EV71 replication was investigated by high-throughput sequencing,luciferase reporter gene assay and Western Blot.The results showed that the expression of has-miR-200 b increased significantly in host cells after EV71 infection by high-throughput miRNA sequencing,and specific inhibition of miR-200 b expression could inhibit EV71 replication.Luciferase reporter gene assay showed that miR-200 b could directly target the 3′-UTR region of IFIT5.Further study confirmed that the increased expression of miR-200 b induced by EV71 infection could inhibit IFIT5 expression and thus supress the type I interferon response.It is shown that EV71 infection can induce the increase of miR-200 b expression in host cells and then inhibit the expression of IFIT5,resulting in the inhibition of intracellular interferon response,which facilitates EV71 replication.

关 键 词：肠道病毒71型 手-足口病 miR-200b IFIT5 干扰素应答 病毒复制 

分 类 号：Q78[生物学—分子生物学] R373.2[医药卫生—病原生物学]