Hopcraft Sharon E, Damania Blossom
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Philos Trans R Soc Lond B Biol Sci. 2017 Oct 19;372(1732). doi: 10.1098/rstb.2016.0267.
Host cells sense viral infection through pattern recognition receptors (PRRs), which detect pathogen-associated molecular patterns (PAMPs) and stimulate an innate immune response. PRRs are localized to several different cellular compartments and are stimulated by viral proteins and nucleic acids. PRR activation initiates signal transduction events that ultimately result in an inflammatory response. Human tumour viruses, which include Kaposi's sarcoma-associated herpesvirus, Epstein-Barr virus, human papillomavirus, hepatitis C virus, hepatitis B virus, human T-cell lymphotropic virus type 1 and Merkel cell polyomavirus, are detected by several different PRRs. These viruses engage in a variety of mechanisms to evade the innate immune response, including downregulating PRRs, inhibiting PRR signalling, and disrupting the activation of transcription factors critical for mediating the inflammatory response, among others. This review will describe tumour virus PAMPs and the PRRs responsible for detecting viral infection, PRR signalling pathways, and the mechanisms by which tumour viruses evade the host innate immune system.This article is part of the themed issue 'Human oncogenic viruses'.
宿主细胞通过模式识别受体（PRRs）感知病毒感染，这些受体可检测病原体相关分子模式（PAMPs）并刺激先天免疫反应。PRRs定位于几个不同的细胞区室，并被病毒蛋白和核酸激活。PRR激活引发信号转导事件，最终导致炎症反应。几种不同的PRRs可检测人类肿瘤病毒，其中包括卡波西肉瘤相关疱疹病毒、爱泼斯坦-巴尔病毒、人乳头瘤病毒、丙型肝炎病毒、乙型肝炎病毒、1型人类嗜T细胞病毒和默克尔细胞多瘤病毒。这些病毒采用多种机制逃避先天免疫反应，包括下调PRRs、抑制PRR信号传导以及破坏对介导炎症反应至关重要的转录因子的激活等。本综述将描述肿瘤病毒PAMPs以及负责检测病毒感染的PRRs、PRR信号通路，以及肿瘤病毒逃避宿主先天免疫系统的机制。本文是主题为“人类致癌病毒”的特刊的一部分。
