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Interplay between Interferon-Mediated Innate Immunity and Porcine Reproductive and Respiratory Syndrome Virus

机译:干扰素介导的先天免疫力与猪繁殖与呼吸综合征病毒之间的相互作用

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摘要

Innate immunity is the first line of defense against viral infection, and in turn, viruses have evolved to evade host immune surveillance. As a result, viruses may persist in host and develop chronic infections. Type I interferons (IFN-α/β) are among the most potent antiviral cytokines triggered by viral infections. Porcine reproductive and respiratory syndrome (PRRS) is a disease of pigs that is characterized by negligible induction of type I IFNs and viral persistence for an extended period. For IFN production, RIG-I/MDA5 and JAK-STAT pathways are two major signaling pathways, and recent studies indicate that PRRS virus is armed to modulate type I IFN responses during infection. This review describes the viral strategies for modulation of type I IFN responses. At least three non–structural proteins (Nsp1, Nsp2, and Nsp11) and a structural protein (N nucleocapsid protein) have been identified and characterized to play roles in the IFN suppression and NF-κB pathways. Nsp’s are early proteins while N is a late protein, suggesting that additional signaling pathways may be involved in addition to the IFN pathway. The understanding of molecular bases for virus-mediated modulation of host innate immune signaling will help us design new generation vaccines and control PRRS.
机译:先天性免疫是抵抗病毒感染的第一道防线,而病毒又进化出逃避宿主免疫监视的能力。结果,病毒可能会在宿主体内持续存在并发展为慢性感染。 I型干扰素(IFN-α/β)是由病毒感染触发的最有效的抗病毒细胞因子之一。猪繁殖与呼吸综合症(PRRS)是一种猪疾病,其特征在于I型IFN的诱导可忽略不计,并且病毒的持久性持续时间较长。对于IFN的产生,RIG-I / MDA5和JAK-STAT通路是两个主要的信号通路,最近的研究表明PRRS病毒可在感染过程中调节I型IFN反应。这篇综述描述了调节I型IFN反应的病毒策略。至少已鉴定出三种非结构蛋白(Nsp1,Nsp2和Nsp11)和一种结构蛋白(N核衣壳蛋白),并在干扰素抑制和NF-κB途径中发挥作用。 Nsp是早期蛋白,而N是晚期蛋白,表明除IFN途径外,可能还涉及其他信号途径。对病毒介导的宿主固有免疫信号调节分子基础的理解将有助于我们设计新一代疫苗和控制PRRS。

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