Antiviral innate immunity and stress granule responses.

Antiviral innate immunity and stress granule responses.
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DOI:
10.1016/j.it.2014.07.006
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发表时间:
2014-09
影响因子:
16.8
通讯作者:
Fujita T
Fujita T
中科院分区:
医学1区
文献类型:
--
作者:
Onomoto K;Yoneyama M;Fung G;Kato H;Fujita T

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应激颗粒(SGS)是在感染某些DNA和RNA病毒后产生的。许多病毒阻止了SG的诱导,尽管有些病毒似乎受益于SG的形成。一些与生俱来的免疫感受器与SG有关,但这如何影响功能尚不清楚。证据表明,SG的形成是抗病毒反应的一个重要方面。病毒感染触发哺乳动物细胞中抗病毒先天免疫反应的激活。细胞质中的病毒RNA激活信号通路,导致干扰素(IFN)和干扰素刺激基因的产生。一些病毒感染可诱导细胞质颗粒聚集,类似于动态核糖核蛋白聚集,被称为应激颗粒(SGS),这表明这些病毒可能利用这种应激反应来获取自身的利益。相比之下,一些病毒主动抑制SG的形成,表明这些结构具有抗病毒功能。我们就不同病毒感染与SG形成的关系作一综述。我们研究了SGS抗病毒功能的证据,并强调了了解细胞对病毒感染的应激反应的重要领域。
Stress granules (SGs) are induced upon infection with some DNA and RNA viruses. Many viruses block the induction of SG, although some appear to benefit from SG formation. Some innate immune sensors associate with SG, but how this affects function is unclear. The evidence suggests that SG formation is an important aspect of the antiviral response. Viral infection triggers the activation of antiviral innate immune responses in mammalian cells. Viral RNA in the cytoplasm activates signaling pathways that result in the production of interferons (IFNs) and IFN-stimulated genes. Some viral infections have been shown to induce cytoplasmic granular aggregates similar to the dynamic ribonucleoprotein aggregates termed stress granules (SGs), suggesting that these viruses may utilize this stress response for their own benefit. By contrast, some viruses actively inhibit SG formation, suggesting an antiviral function for these structures. We review here the relationship between different viral infections and SG formation. We examine the evidence for antiviral functions for SGs and highlight important areas of inquiry towards understanding cellular stress responses to viral infection.
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