Web of interferon stimulated antiviral factors to control the influenza A viruses replication
Web of interferon stimulated antiviral factors to control the influenza A viruses replication
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DOI：
10.1016/j.micpath.2019.103919
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发表时间：
2020-02-01
影响因子：
3.8
通讯作者：
Rahman, Sajjad Ur
中科院分区：
文献类型：
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作者：
Goraya, Mohsan Ullah;Zaighum, Fozia;Rahman, Sajjad Ur
流感病毒在全世界的动物和人类中引起轻度至重度感染，具有显着的发病率和死亡率。甲型流感病毒感染真核细胞，通过模式识别受体（PRR）和病原体相关分子模式（PAMP）之间的相互作用触发先天免疫系统的诱导，最终诱导干扰素（IFN）。因此，干扰素与其细胞膜上的同源受体结合，并通过 Janus 激酶信号转导器和转录激活剂 (JAK-STAT) 途径激活干扰素刺激基因 (ISG) 转录调节的信号传导途径。这些 ISG 的累积作用建立了宿主的抗病毒状态。已经描述了几种 ISG，它们在病毒生命周期的多个步骤中对抑制甲型流感病毒的感染和复制发挥着关键作用。在这篇综述中，讨论了这些 ISG 对抗甲型流感病毒的动态和冗余。此外，对 ISG 在流感病毒发病机制中作用的当前理解和分子机制进行了严格审查。
Influenza viruses cause mild to severe infections in animals and humans worldwide with significant morbidity and mortality. Infection of eukaryotic cells with influenza A viruses triggers the induction of innate immune system through the interaction between pattern recognition receptors (PRRs) and pathogen associated molecular patterns (PAMPs), which culminate in the induction of interferons (IFNs). Consequently, IFNs bind to their cognate receptors on the cellular membrane and activate the signaling pathway for transcriptional regulation of interferon-stimulated genes (ISGs) through Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. Cumulative actions of these ISGs establish an antiviral state of the host. Several ISGs have been described, which play critical roles to inhibit the infection and replication of influenza A viruses at multiple steps of virus life cycle. In this review, the dynamics and redundancy of these ISGs against influenza A viruses are discussed. Additionally, current understanding and molecular mechanisms that are underlying the roles of ISGs in pathogenesis of influenza virus are critically reviewed.