Regulation of innate immune responses by rabies virus.
Regulation of innate immune responses by rabies virus.
复制标题
狂犬病病毒对先天免疫反应的调节
DOI：
10.1002/ame2.12273
复制
发表时间：
2022-10
影响因子：
3.7
通讯作者：
Wang, Hualei
中科院分区：
文献类型：
--
作者：
Zhang, Haili;Huang, Jingbo;Song, Yumeng;Liu, Xingqi;Qian, Meichen;Huang, Pei;Li, Yuanyuan;Zhao, Ling;Wang, Hualei
狂犬病病毒（RABV）是一种传染性、嗜神经性病原体，引起狂犬病并感染人类和几乎所有温血动物，对人类和公共安全构成巨大威胁。众所周知，先天免疫是宿主抵御病毒感染的关键第一道防线。它通过模式识别受体识别病原体相关分子模式和危险相关分子模式来监测入侵的病原体，从而产生I型干扰素（IFNα/β）、炎症细胞因子和趋化因子，或激活自噬或细胞凋亡来抑制病毒复制。就 RABV 而言，当皮肤或肌肉被咬伤或抓伤时，通常会触发先天免疫反应。然而，RABV已经进化出多种方式来逃避甚至劫持先天免疫反应来完成自身复制并最终侵入中枢神经系统（CNS）。 RABV 一旦到达中枢神经系统，就无法被免疫系统或任何药物消灭。因此，有必要更好地了解 RABV 与先天免疫之间的相互作用，以制定有效的策略来对抗其感染。在此，我们回顾了RABV诱导的先天免疫反应，并阐明了RABV的拮抗机制，为狂犬病的控制提供新的见解。 RABV感染后，宿主先天免疫反应会被激活，调节RABV的复制，包括干扰素反应、自噬、细胞凋亡、炎症反应和线粒体功能障碍。同时，RABV在与宿主共同进化的过程中形成了多种逃逸策略，主要是通过病毒蛋白P、M、N调节宿主先天免疫通路来促进自我复制。
Rabies virus (RABV) is an infectious and neurotropic pathogen that causes rabies and infects humans and almost all warm‐blooded animals, posing a great threat to people and public safety. It is well known that innate immunity is the critical first line of host defense against viral infection. It monitors the invading pathogens by recognizing the pathogen‐associated molecular patterns and danger‐associated molecular patterns through pattern‐recognition receptors, leading to the production of type I interferons (IFNα/β), inflammatory cytokines, and chemokines, or the activation of autophagy or apoptosis to inhibit virus replication. In the case of RABV, the innate immune response is usually triggered when the skin or muscle is bitten or scratched. However, RABV has evolved many ways to escape or even hijack innate immune response to complete its own replication and eventually invades the central nervous system (CNS). Once RABV reaches the CNS, it cannot be wiped out by the immune system or any drugs. Therefore, a better understanding of the interplay between RABV and innate immunity is necessary to develop effective strategies to combat its infection. Here, we review the innate immune responses induced by RABV and illustrate the antagonism mechanisms of RABV to provide new insights for the control of rabies. Host innate immune response will be activated upon RABV infection to regulate the replication of RABV, including interferon response, autophagy, apoptosis, inflammatory response, and mitochondrial dysfunction. Meanwhile, RABV has formed a variety of escape strategies in the process of co‐evolution with hosts, mainly through regulating host innate immune pathways by viral proteins P, M, and N to promote self‐replication.
影响因子：
1.4
作者：
Mujibur Rahaman M;Siddiqi UR;Sabuj AAM;Ahmed BN;Tahmina S;Faruque MR;Ghosh S;Uddin N
通讯作者：
Uddin N