Viral evasion of intracellular DNA and RNA sensing.
Viral evasion of intracellular DNA and RNA sensing.
复制标题
病毒逃避细胞内 DNA 和 RNA 的感应。
DOI：
10.1038/nrmicro.2016.45
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发表时间：
2016-06
期刊：
影响因子：
--
通讯作者：
中科院分区：
文献类型：
--
作者：
种系编码的模式识别受体（PRR）介导针对病毒病原体的早期先天免疫反应。视黄酸诱导基因 I 蛋白 (RIG-I) 和黑色素瘤分化相关蛋白 5 (MDA5) 是细胞质传感器，可检测病毒 RNA 种类并通过线粒体抗病毒信号蛋白 (MAVS) 发出信号，以诱导 I 型干扰素 (IFN) 和其他细胞因子的产生。细胞内 DNA 传感器，例如环 GMP-AMP 合酶 (cGAS) 和 IFNγ 诱导蛋白 16 (IFI16)，可检测细胞质和/或细胞核中的病毒 DNA，并通过 IFN 基因刺激剂 (STING) 发出信号以触发免疫反应。病毒通过隔离或修饰其病毒基因组以及通过操纵 PRR 或其接头蛋白的翻译后修饰来拮抗 PRR。一些病毒会裂解或降解 PRR 或其接头，或者隔离并重新定位 PRR 以逃避免疫。更好地了解细胞免疫监视机制和病毒免疫逃避策略可能会指导抗病毒疗法和疫苗的开发。本文的在线版本 (doi:10.1038/nrmicro.2016.45) 包含补充材料，可供授权用户使用。模式识别受体（PRR）检测病毒病原体的保守分子特征，并启动导致抗病毒基因表达的信号传导。在这篇综述中，Chan 和 Gack 重点介绍了细胞内病毒 RNA 和 DNA 传感器的主要类别，并讨论了用于逃避这些传感器免疫监视的病毒策略。本文的在线版本 (doi:10.1038/nrmicro.2016.45) 包含补充材料，可供授权用户使用。病毒与其宿主的共同进化导致了善于逃避或主动抑制宿主免疫的病毒病原体的出现。模式识别受体 (PRR) 是抗病毒免疫的关键组成部分，可检测病毒病原体的保守分子特征并启动导致抗病毒基因表达的信号传导。在这篇综述中，我们讨论了病毒用来逃避病毒 RNA 或 DNA 关键细胞内传感器免疫监视的策略，重点关注 RIG-I 样受体 (RLR)、环 GMP-AMP 合酶 (cGAS) 和干扰素-γ (IFNγ) 诱导蛋白 16 (IFI16)。此类病毒策略包括病毒核酸的隔离或修饰、干扰PRR或其衔接蛋白的特异性翻译后修饰、PRR或其衔接蛋白的降解或切割以及PRR的隔离或重新定位。在分子水平上了解病毒免疫逃避机制可能会指导疫苗和抗病毒药物的开发。本文的在线版本 (doi:10.1038/nrmicro.2016.45) 包含补充材料，可供授权用户使用。
Germline-encoded pattern recognition receptors (PRRs) mediate an early innate immune response against viral pathogens. Retinoic acid-inducible gene I protein (RIG-I) and melanoma differentiation-associated protein 5 (MDA5) are cytoplasmic sensors that detect viral RNA species and signal through the mitochondrial antiviral-signalling protein (MAVS) to induce the production of type I interferons (IFNs) and other cytokines. Intracellular DNA sensors, such as cyclic GMP–AMP synthase (cGAS) and IFNγ-inducible protein 16 (IFI16), detect viral DNA in the cytoplasm and/or nucleus and signal through the stimulator of IFN genes (STING) to trigger an immune response. Viruses antagonize PRRs through the sequestration or modification of their viral genomes and through the manipulation of post-translational modifications of PRRs or their adaptor proteins. Some viruses cleave or degrade PRRs or their adaptors, or sequester and relocalize PRRs to escape immunity. A better understanding of the cellular immune-surveillance machinery and viral immune evasion strategies may guide the development of antiviral therapeutics and vaccines. The online version of this article (doi:10.1038/nrmicro.2016.45) contains supplementary material, which is available to authorized users. Pattern recognition receptors (PRRs) detect conserved molecular features of viral pathogens and initiate signalling that results in the expression of antiviral genes. In this Review, Chan and Gack highlight the major classes of intracellular viral RNA and DNA sensors and discuss the viral strategies that are used to escape immune surveillance by those sensors. The online version of this article (doi:10.1038/nrmicro.2016.45) contains supplementary material, which is available to authorized users. The co-evolution of viruses with their hosts has led to the emergence of viral pathogens that are adept at evading or actively suppressing host immunity. Pattern recognition receptors (PRRs) are key components of antiviral immunity that detect conserved molecular features of viral pathogens and initiate signalling that results in the expression of antiviral genes. In this Review, we discuss the strategies that viruses use to escape immune surveillance by key intracellular sensors of viral RNA or DNA, with a focus on RIG-I-like receptors (RLRs), cyclic GMP–AMP synthase (cGAS) and interferon-γ (IFNγ)-inducible protein 16 (IFI16). Such viral strategies include the sequestration or modification of viral nucleic acids, interference with specific post-translational modifications of PRRs or their adaptor proteins, the degradation or cleavage of PRRs or their adaptors, and the sequestration or relocalization of PRRs. An understanding of viral immune-evasion mechanisms at the molecular level may guide the development of vaccines and antivirals. The online version of this article (doi:10.1038/nrmicro.2016.45) contains supplementary material, which is available to authorized users.
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