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针对非节段性负链RNA病毒的固有免疫反应。

Innate immune response against nonsegmented negative strand RNA viruses.

作者信息

Bose Santanu, Banerjee Amiya K

机构信息

Department of Virology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA.

出版信息

J Interferon Cytokine Res. 2003 Aug;23(8):401-12. doi: 10.1089/107999003322277810.

Abstract

Innate immune response represents the hallmark of host defense against foreign pathogens, including viruses. Not only does this response combat viruses during initial stages of infection, but it shapes the adaptive immune response as well. This review focuses on this critical host defense mechanism, the innate immune response, in the context of infection by nonsegmented negative strand RNA viruses of the Paramyxoviridae family. We specifically focus on the two critical transcription factors, nuclear factor-kappaB (NF-kappaB) and interferon (IFN) regulatory factor-3 (IRF-3), that play an important role in establishing an innate antiviral state. The antiviral cytokine IFN-alpha/beta (IFN type I) produced following viral infection as a result of activation of NF-kappaB or IRF-3 or both exerts an antiviral state by inducing the Janus kinases/signal transducer and activator (Jak-Stat) pathway. In that context, our review discusses various strategies adopted by these viruses to counteract and evade the antiviral action of IFN I for replicative advantages, especially after modulation of the Jak-Stat antiviral pathway. Understanding this interplay between the innate immune response and viral replication is fundamental to probing into the molecular basis of host-virus interaction.

摘要

固有免疫反应是宿主抵御包括病毒在内的外来病原体的标志。这种反应不仅在感染的初始阶段对抗病毒,还塑造适应性免疫反应。本综述聚焦于副黏病毒科非节段性负链RNA病毒感染背景下这一关键的宿主防御机制——固有免疫反应。我们特别关注在建立固有抗病毒状态中起重要作用的两个关键转录因子,即核因子-κB(NF-κB)和干扰素(IFN)调节因子-3(IRF-3)。病毒感染后,由于NF-κB或IRF-3或两者激活而产生的抗病毒细胞因子IFN-α/β(I型干扰素),通过诱导Janus激酶/信号转导子和激活子(Jak-Stat)途径发挥抗病毒状态。在此背景下,我们的综述讨论了这些病毒为获得复制优势而采取的各种策略,以对抗和逃避I型干扰素的抗病毒作用,尤其是在调节Jak-Stat抗病毒途径之后。了解固有免疫反应与病毒复制之间的这种相互作用对于探究宿主-病毒相互作用的分子基础至关重要。

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