生物学杂志

生物学杂志 ›› 2022, Vol. 39 ›› Issue (5): 21-.doi: 10.3969/j.issn.2095-1736.2022.05.021

• 研究报告 • 上一篇    下一篇

EV71诱导has-miR-200b表达并促进自身复制的机制

  

  1. 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
  • 出版日期:2022-10-18 发布日期:2022-10-18
  • 通讯作者: 傅煜轩，博士，副教授，主要从事感染与免疫研究，E-mail：fuyx@suda.edu.cn
  • 作者简介:胡静平，硕士，高级实验师，从事感染与免疫研究，E-mail：jingpinghu@suda.edu.cn；王燕，硕士，口腔科住院医师，从事口腔感染及正畸研究，E-mail: wooyan@yeah.net；胡静平和王燕为共同第一作者
  • 基金资助:
    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

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

  1. 1. Institutes of Biology and Medical Sciences, Soochow University,
    Suzhou 215123, China; 2. Department of Stomatology, Affiliated Suzhou Hospital of Nanjing Medical University,
    Suzhou Municipal Hospital, Suzhou 215001, China
  • Online:2022-10-18 Published:2022-10-18

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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。

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

Abstract: The role of miR-200b 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-200b increased significantly in host cells after EV71 infection by high-throughput miRNA sequencing, and specific inhibition of miR-200b expression could inhibit EV71 replication. Luciferase reporter gene assay showed that miR-200b could directly target the 3′-UTR region of IFIT5. Further study confirmed that the increased expression of miR-200b 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-200b expression in host cells and then inhibit the expression of IFIT5, resulting in the inhibition of intracellular interferon response, which facilitates EV71 replication.

Key words: EV71;hand-foot-and-mouth disease;miR-200b;IFIT5, interferon response;virus replication

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