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.

中文翻译：

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小核糖核酸病毒的先天免疫逃避。

家庭Picornaviridae包含大量可导致广泛宿主疾病的病毒，这些病毒已引起全球范围内严重的公共卫生问题，并导致巨大的经济负担。对小核糖核酸病毒感染期间病毒-宿主相互作用的全面了解将有助于预防和治愈这些疾病。微小RNA病毒感染后，宿主病原体识别受体（PRR）感知病毒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，从而导致多种激酶和转录因子的激活，并有助于随后表达干扰素（IFN），IFN诱导的抗病毒基因以及各种炎性细胞因子和趋化因子。 。相反，为了维持病毒复制和传播，微小核糖核酸病毒已经进化出多种巧妙的策略来阻断先天免疫信号传导并阻碍宿主抗病毒反应。在这篇评论中，我们将总结家庭成员的最新进展Picornaviridae通过逃避PRR检测，阻断衔接子分子和激酶的激活，破坏转录因子以及抗病毒限制因子的抵抗作用来抵消宿主的免疫反应。这种免疫逃逸的知识将帮助我们更好地了解小核糖核酸病毒的发病机理，并为开发抗病毒策略和改进疫苗提供见识。