Castanier Céline, Arnoult Damien
INSERM U1014, Hopital Paul Brousse, Batiment Lavoisier, 14 avenue Paul Vaillant Couturier, 94807 Villejuif cedex, France.
Biochim Biophys Acta. 2011 Apr;1813(4):575-83. doi: 10.1016/j.bbamcr.2010.08.009. Epub 2010 Aug 31.
Viruses have developed a battery of distinct strategies to overcome the very sophisticated defense mechanisms of the infected host. Throughout the process of pathogen-host co-evolution, viruses have therefore acquired the capability to prevent host cell apoptosis because elimination of infected cells via apoptosis is one of the most ancestral defense mechanism against infection. Conversely, induction of apoptosis may favor viral dissemination as a result of the dismantlement of the infected cells. Mitochondria have been long recognized for their key role in the modulation of apoptosis but more recently, mitochondria have been shown to serve as a crucial platform for innate immune signaling as illustrated by the identification of MAVS. Thus, it is therefore not surprising that this organelle represents a recurrent target for viruses, aiming to manipulate the fate of the infected host cell or to inhibit innate immune response. In this review, we highlight the viral proteins that are specifically targeted to the mitochondria to subvert host defense. This article is part of a Special Issue entitled Mitochondria: the deadly organelle.
病毒已经发展出一系列独特的策略来克服被感染宿主非常复杂的防御机制。因此,在病原体与宿主共同进化的过程中,病毒获得了防止宿主细胞凋亡的能力,因为通过凋亡消除被感染细胞是对抗感染的最原始防御机制之一。相反,由于被感染细胞的解体,诱导凋亡可能有利于病毒传播。长期以来,线粒体因其在凋亡调节中的关键作用而被认可,但最近,线粒体已被证明是天然免疫信号传导的关键平台,如MAVS的发现所示。因此,这个细胞器成为病毒反复靶向的目标也就不足为奇了,病毒旨在操纵被感染宿主细胞的命运或抑制天然免疫反应。在这篇综述中,我们重点介绍了专门靶向线粒体以颠覆宿主防御的病毒蛋白。本文是名为“线粒体:致命细胞器”的特刊的一部分。