Center for Molecular Virology, CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, PR China; University of the Chinese Academy of Sciences, Beijing, 100101, PR China.
Center for Molecular Virology, CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, PR China.
Biochem Biophys Res Commun. 2014 May 9;447(3):550-5. doi: 10.1016/j.bbrc.2014.04.021. Epub 2014 Apr 13.
Exposure of cells to type I interferon (IFN) induces an antiviral state that prevents viral infection, but viruses can utilize multiple tactics to antagonize the host immune system. Enterovirus 71 (EV71) and Coxsackievirus A16 (CVA16) are two major pathogens that cause hand, foot, and mouth disease (HFMD), which is prevalent among children. We found that both EV71 and CA16 have different reactions to type I IFN pretreatment and induction patterns of type I IFN on Rhabdomyosarcoma (RD) cells. Further, a human-α and β IFN PCR array was employed to analyze the expressions of 84 genes related to the type I IFN pathway. We found significant up-regulation of multiple genes in the presence of type I IFN and differential regulation patterns during EV71 or CA16 infection in RD cells. For instance, EV71 infection repressed the JAK-STAT signaling pathway and interferon-stimulated gene (ISG) expression, whereas CA16 infection normally triggers the JAK-STAT pathway, leading to the expression of ISGs. Taken together, this study provides a comprehensive view of the differential impacts of EV71 and CA16 infection on 84 genes in the IFN pathway, shedding light on the different resistances of these viruses to type I IFN treatment and cytotoxic effects in RD cells.
细胞暴露于 I 型干扰素（IFN）会诱导抗病毒状态，从而阻止病毒感染，但病毒可以利用多种策略来拮抗宿主免疫系统。肠道病毒 71 型（EV71）和柯萨奇病毒 A16 型（CVA16）是引起手足口病（HFMD）的两种主要病原体，HFMD 在儿童中很常见。我们发现 EV71 和 CA16 对 I 型 IFN 预处理有不同的反应，以及 I 型 IFN 对横纹肌肉瘤（RD）细胞诱导的模式也不同。此外，我们还使用了人类-α和-β IFN PCR 阵列来分析与 I 型 IFN 途径相关的 84 个基因的表达。我们发现，在存在 I 型 IFN 的情况下，多个基因的表达显著上调，并且在 RD 细胞中 EV71 或 CA16 感染时呈现出不同的调控模式。例如，EV71 感染抑制了 JAK-STAT 信号通路和干扰素刺激基因（ISG）的表达，而 CA16 感染通常会触发 JAK-STAT 通路，导致 ISG 的表达。总之，本研究全面展示了 EV71 和 CA16 感染对 IFN 途径中 84 个基因的不同影响，揭示了这些病毒对 I 型 IFN 治疗和 RD 细胞细胞毒性作用的不同抵抗力。
