Blondel Danielle, Maarifi Ghizlane, Nisole Sébastien, Chelbi-Alix Mounira K
Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS UMR 9198, Université Paris-Sud, Gif-sur-Yvette 91190, France.
INSERM UMR-S 1124, Université Paris Descartes, Centre Interdisciplinaire Chimie Biologie-Paris (FR 3567, CNRS), 75270 Paris Cedex 6, France.
Viruses. 2015 Jul 7;7(7):3675-702. doi: 10.3390/v7072794.
Interferon (IFN) treatment induces the expression of hundreds of IFN-stimulated genes (ISGs). However, only a selection of their products have been demonstrated to be responsible for the inhibition of rhabdovirus replication in cultured cells; and only a few have been shown to play a role in mediating the antiviral response in vivo using gene knockout mouse models. IFNs inhibit rhabdovirus replication at different stages via the induction of a variety of ISGs. This review will discuss how individual ISG products confer resistance to rhabdoviruses by blocking viral entry, degrading single stranded viral RNA, inhibiting viral translation or preventing release of virions from the cell. Furthermore, this review will highlight how these viruses counteract the host IFN system.
干扰素(IFN)治疗可诱导数百种干扰素刺激基因(ISG)的表达。然而,仅证实其部分产物可抑制培养细胞中的弹状病毒复制;并且仅少数产物在使用基因敲除小鼠模型的体内抗病毒反应中发挥作用。干扰素通过诱导多种ISG在不同阶段抑制弹状病毒复制。本综述将讨论单个ISG产物如何通过阻断病毒进入、降解单链病毒RNA、抑制病毒翻译或阻止病毒粒子从细胞中释放来赋予对弹状病毒的抗性。此外,本综述将强调这些病毒如何对抗宿主干扰素系统。