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首页> 美国卫生研究院文献>Microorganisms >Inhibition of Type III Interferon Expression in Intestinal Epithelial Cells—A Strategy Used by Coxsackie B Virus to Evade the Host’s Innate Immune Response at the Primary Site of Infection?
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Inhibition of Type III Interferon Expression in Intestinal Epithelial Cells—A Strategy Used by Coxsackie B Virus to Evade the Host’s Innate Immune Response at the Primary Site of Infection?

机译：抑制III型干扰素在肠上皮细胞中的表达 - 柯萨基B病毒用于避免宿主在感染初始部位的宿主的策略？

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摘要

Increasing evidence highlights the importance of the antiviral activities of the type III interferons (IFNλs; IL-28A, IL-28B, IL29, and IFNλ4) in the intestine. However, many viruses have developed strategies to counteract these defense mechanisms by preventing the production of IFNs. Here we use infection models, a clinical virus isolate, and several molecular biology techniques to demonstrate that both type I and III IFNs induce an antiviral state and attenuate Coxsackievirus group B (CVB) replication in human intestinal epithelial cells (IECs). While treatment of IECs with a viral mimic (poly (I:C)) induced a robust expression of both type I and III IFNs, no such up-regulation was observed after CVB infection. The blunted IFN response was paralleled by a reduction in the abundance of proteins involved in the induction of interferon gene transcription, including TIR-domain-containing adapter-inducing interferon-β (TRIF), mitochondrial antiviral-signaling protein (MAVS), and the global protein translation initiator eukaryotic translation initiation factor 4G (eIF4G). Taken together, this study highlights a potent anti-Coxsackieviral effect of both type I and III IFNs in cells located at the primary site of infection. Furthermore, we show for the first time that the production of type I and III IFNs in IECs is blocked by CVBs. These findings suggest that CVBs evade the host immune response in order to successfully infect the intestine.
机译：越来越多的证据突出了III型干扰素（IFNλsss;IFNλs; IL-28a，IL-28b，IL29和IFNλ4）的抗病毒活性的重要性。然而，许多病毒通过防止产生IFNS来抵消这些防御机制的策略。在这里，我们使用感染模型，临床病毒分离物和几种分子生物学技术，以证明I型和III IFNS诱导人类肠上皮细胞（IEC）中的抗病毒状态并衰减CoxSackeivirus Group B（CVB）复制。同时用病毒模拟物（Poly（I：C））诱导IEC的IEC，诱导I型和III IFNS的稳健表达，在CVB感染后没有观察到这种上调。钝化的IFN响应被诱导干扰素基因转录所涉及的蛋白质的丰度降低，包括含TIR-结构域的适配器诱导的干扰素-β（TRIF），线粒体抗病毒性信号蛋白（MAV）和全局蛋白翻译引发剂真核翻译开始因子4G（EIF4G）。在一起，该研究突出了位于感染初级部位的细胞中I和III IFNS两种I和III IFNS的有效的抗Coxsackieviral效果。此外，我们首次展示IECS中I和III IFNS的生产被CVBS阻止。这些研究结果表明，CVBS避免了宿主免疫应答，以便成功地感染肠道。

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