Jing Zhi-Zhong, He Xiao-Bing, Fang Yong-Xiang, Jia Huai-Jie, Zhou Tao
State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Veterinary Public Health of Agricultural Ministry, Lanzhou Veterinary Research Institute, CAAS, Lanzhou 730046, China.
Bing Du Xue Bao. 2012 Jun;28(4):453-61.
Toll-like receptors (TLRs) are germline-encoded pattern recognition receptors (PRRs) that play a central role in host cell recognition and responses to virus infection, leading to the production of interferons (IFNs) and proinflammatory cytokines. In parallel, in order to establish an infection, viruses have to develop exclusively strategies to interfere with TLRs signaling, particularly some important adaptors activation such as MyD88, NF-kappaB, TRIF and IRFs, and suppress or escape host's antiviral immune response. In this paper, we review the latest findings on the various strategies used by viruses to modulate TLRs-mediated innate immune response, with special emphasis on immune evasion mechanism of VACV, HCV and HIV. By highlighting recent progress in these areas, we hope to convey a greater understanding of how viruses hamper TLRs signaling and how to overcome viral infection.
Toll样受体(TLRs)是种系编码的模式识别受体(PRRs),在宿主细胞识别和对病毒感染的反应中起核心作用,导致干扰素(IFNs)和促炎细胞因子的产生。与此同时,为了建立感染,病毒必须专门制定策略来干扰TLRs信号传导,特别是一些重要衔接蛋白的激活,如髓样分化因子88(MyD88)、核因子κB(NF-κB)、TIR结构域衔接蛋白诱导干扰素β(TRIF)和干扰素调节因子(IRFs),并抑制或逃避宿主的抗病毒免疫反应。在本文中,我们综述了病毒用于调节TLRs介导的先天免疫反应的各种策略的最新发现,特别强调了痘苗病毒(VACV)、丙型肝炎病毒(HCV)和人类免疫缺陷病毒(HIV)的免疫逃逸机制。通过突出这些领域的最新进展,我们希望能让人们更深入地了解病毒如何阻碍TLRs信号传导以及如何克服病毒感染。