Chatterjee Srirupa, Basler Christopher F, Amarasinghe Gaya K, Leung Daisy W
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Center of Microbial Pathogenesis, Georgia State University, Atlanta, GA 30303, USA.
J Mol Biol. 2016 Aug 28;428(17):3467-82. doi: 10.1016/j.jmb.2016.07.017. Epub 2016 Jul 31.
The host innate immune system serves as the first line of defense against viral infections. Germline-encoded pattern recognition receptors detect molecular patterns associated with pathogens and activate innate immune responses. Of particular relevance to viral infections are those pattern recognition receptors that activate type I interferon responses, which establish an antiviral state. The order Mononegavirales is composed of viruses that possess single-stranded, non-segmented negative-sense (NNS) RNA genomes and are important human pathogens that consistently antagonize signaling related to type I interferon responses. NNS viruses have limited encoding capacity compared to many DNA viruses, and as a likely consequence, most open reading frames encode multifunctional viral proteins that interact with host factors in order to evade host cell defenses while promoting viral replication. In this review, we will discuss the molecular mechanisms of innate immune evasion by select NNS viruses. A greater understanding of these interactions will be critical in facilitating the development of effective therapeutics and viral countermeasures.
宿主先天免疫系统是抵御病毒感染的第一道防线。种系编码的模式识别受体检测与病原体相关的分子模式并激活先天免疫反应。与病毒感染特别相关的是那些激活I型干扰素反应的模式识别受体,该反应建立抗病毒状态。单股负链RNA病毒目由具有单链、不分节段的负链(NNS)RNA基因组的病毒组成,并且是持续拮抗与I型干扰素反应相关信号传导的重要人类病原体。与许多DNA病毒相比,NNS病毒的编码能力有限,并且可能因此,大多数开放阅读框编码多功能病毒蛋白,这些蛋白与宿主因子相互作用,以逃避宿主细胞防御同时促进病毒复制。在本综述中,我们将讨论特定NNS病毒逃避先天免疫的分子机制。对这些相互作用的更深入理解对于促进有效治疗方法和病毒对策的开发至关重要。