Schröder M, Bowie A G
Viral Immune Evasion Group, School of Biochemistry and Immunology, Trinity College Dublin, Dublin 2, Ireland.
Biochem Soc Trans. 2007 Dec;35(Pt 6):1512-4. doi: 10.1042/BST0351512.
Viral recognition is mediated by different classes of PRRs (pattern-recognition receptors) among which the TLRs (Toll-like receptors) and the RLHs [RIG (retinoic-acid-inducible)-like helicases] play major roles. The detection of PAMPs (pathogen-associated molecular patterns) by these PRRs leads to the initiation of signalling pathways that ultimately result in the activation of transcription factors such as NF-kappaB (nuclear factor kappaB) and IRF-3 [IFN (interferon) regulatory factor-3] and IRF-7 and the induction of pro-inflammatory cytokines and type I IFNs. Viruses have evolved a fine-tuned mechanism to evade detection by the immune system or to interfere with the resulting signalling pathways. Here, we discuss viral evasion proteins that specifically interfere with TLR and/or RLH signalling.
病毒识别由不同类别的模式识别受体（PRR）介导，其中Toll样受体（TLR）和视黄酸诱导基因I样解旋酶（RLH）发挥主要作用。这些PRR对病原体相关分子模式（PAMP）的检测会引发信号通路的启动，最终导致转录因子如核因子κB（NF-κB）、干扰素调节因子3（IRF-3）和IRF-7的激活，以及促炎细胞因子和I型干扰素的诱导。病毒已经进化出一种精细调节的机制来逃避免疫系统的检测或干扰由此产生的信号通路。在这里，我们讨论特异性干扰TLR和/或RLH信号传导的病毒逃避蛋白。
