Feng Na, Zhou Zhizhao, Li Yuanxia, Zhao Lifang, Xue Zhengfeng, Lu Rong, Jia Kunpeng
Department of Pediatrics, Affiliated Hospital of Yanan University, China.
Neonatology Department, Yangling Demonstration Zone Hospital, China.
Virus Res. 2017 Jun 2;237:27-36. doi: 10.1016/j.virusres.2017.05.008. Epub 2017 May 12.
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.
肠道病毒71型（EV71）是手足口病的病原体，在全球范围内日益成为一项公共卫生挑战。I型干扰素（IFN）是一类重要的细胞因子家族，可调节对病原体的固有免疫和适应性免疫反应。这些信号通路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信号通路以实现增殖和传播。在本研究中，我们证明EV71通过激活微小RNA-21来逃避免疫监视系统以实现增殖。我们证明EV71感染会上调miR-21，进而抑制EV71触发的I型干扰素产生，从而促进EV71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型干扰素产生。
