State Key Laboratory of Veterinary Etiological Biology, National Foot and Mouth Diseases Reference Laboratory, Key Laboratory of Animal Virology of Ministry of Agriculture, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu, P. R. China.
Program in Virology, Division of Medical Sciences, Harvard Medical School, Boston, MA, U.S.A.
Eur J Immunol. 2020 Sep;50(9):1268-1282. doi: 10.1002/eji.202048785. Epub 2020 Aug 23.
The family Picornaviridae comprises a large number of viruses that cause disease in broad spectrum of hosts, which have posed serious public health concerns worldwide and led to significant economic burden. A comprehensive understanding of the virus-host interactions during picornavirus infections will help to prevent and cure these diseases. Upon picornavirus infection, host pathogen recognition receptors (PRRs) sense viral RNA to activate host innate immune responses. The activated PRRs initiate signal transduction through a series of adaptor proteins, which leads to activation of several kinases and transcription factors, and contributes to the consequent expression of interferons (IFNs), IFN-inducible antiviral genes, as well as various inflammatory cytokines and chemokines. In contrast, to maintain viral replication and spread, picornaviruses have evolved several elegant strategies to block innate immune signaling and hinder host antiviral response. In this review, we will summarize the recent progress of how the members of family Picornaviridae counteract host immune response through evasion of PRRs detection, blocking activation of adaptor molecules and kinases, disrupting transcription factors, as well as counteraction of antiviral restriction factors. Such knowledge of immune evasion will help us better understand the pathogenesis of picornaviruses, and provide insights into developing antiviral strategies and improvement of vaccines.
家族 Picornaviridae 包含大量可感染多种宿主的病毒,这些病毒在全球范围内引发了严重的公共卫生问题,并造成了巨大的经济负担。全面了解正粘病毒感染过程中的病毒-宿主相互作用有助于预防和治疗这些疾病。在正粘病毒感染后,宿主病原体识别受体 (PRR) 会识别病毒 RNA 以激活宿主固有免疫反应。激活的 PRR 通过一系列衔接蛋白启动信号转导,从而激活多种激酶和转录因子,并有助于干扰素 (IFN)、IFN 诱导的抗病毒基因以及各种炎症细胞因子和趋化因子的后续表达。相反,为了维持病毒复制和传播,正粘病毒已经进化出几种巧妙的策略来阻止固有免疫信号并阻碍宿主抗病毒反应。在这篇综述中,我们将总结家族 Picornaviridae 成员通过逃避 PRR 检测、阻断衔接分子和激酶的激活、破坏转录因子以及拮抗抗病毒限制因子来抵抗宿主免疫反应的最新进展。对免疫逃避的这种了解将有助于我们更好地理解正粘病毒的发病机制,并为开发抗病毒策略和改进疫苗提供思路。