Enterovirus 71-induced has-miR-21 contributes to evasion of host immune system by targeting MyD88 and IRAK1
Enterovirus 71-induced has-miR-21 contributes to evasion of host immune system by targeting MyD88 and IRAK1
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DOI：
10.1016/j.virusres.2017.05.008
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发表时间：
2017-06-02
期刊：
影响因子：
5
通讯作者：
Jia, Kunpeng
中科院分区：
文献类型：
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作者：
Feng, Na;Zhou, Zhizhao;Jia, Kunpeng
肠病毒71（EV71）是手足口病的病原，已日益成为世界范围内的公共卫生挑战。I型干扰素（ifn）是一个重要的细胞因子家族，可调节对病原体的先天和适应性免疫反应。这些途径受到宿主的严格调控，以防止不适当的细胞反应，但病毒可以调节这些途径增殖和传播。在这项研究中，我们证明了EV71通过激活microRNA-21来逃避免疫监视系统增殖。我们证明EV71感染上调miR-21， miR-21反过来抑制EV71触发的I型IFN的产生，从而促进EV71的复制。此外，我们证明miR-21靶向髓样分化因子88（MyD88）和白细胞介素-1受体相关激酶1(IRAK1)，它们参与ev71诱导的I型IFN的产生。
Enterovirus71(EV71), the etiological agent of hand-foot-and-mouth disease, has increasingly become a public health challenge around the world. Type I interferons (IFNs) are an important family of cytokines that regulate innate and adaptive immune responses to pathogens. These pathways are tightly regulated by the host to prevent an inappropriate cellular response, but viruses can modulate these pathways to proliferate and spread. In this study, we demonstrated that EV71 evades the immune surveillance system to proliferate by activating microRNA-21. We demonstrated that EV71 infection upregulates miR-21, which in turn suppresses EV71-triggered type I IFN production, thus promoting EV71 replication. Furthermore, we demonstrated that miR-21 targets the myeloid differentiation factor 88(MyD88) and interleukin-1 receptor-associated kinase 1(IRAK1), which are involved in EV71-induced type I IFN production.