Viruses as modulators of mitochondrial functions.
Viruses as modulators of mitochondrial functions.
复制标题
DOI：
10.1155/2013/738794
复制
发表时间：
2013
影响因子：
2.2
通讯作者：
Tikoo SK
中科院分区：
文献类型：
--
作者：
Anand SK;Tikoo SK
线粒体是一种多功能的细胞器，具有多种功能，包括能量产生和分配、细胞凋亡、引发宿主免疫反应、引起疾病和衰老。线粒体介导的免疫反应可能是一种进化适应，通过这种适应，线粒体可能阻止了入侵微生物的进入，从而使它们成为细胞的组成部分。这使得它们成为包括病毒在内的所有入侵病原体的目标。病毒以高度特异性的方式诱导或抑制各种线粒体过程，以便它们能够复制和产生后代。一些病毒编码Bcl 2同源物以对抗细胞和线粒体蛋白的促凋亡功能。其他调节渗透性转换孔，并防止或诱导凋亡蛋白从线粒体释放。像单纯疱疹病毒1型这样的病毒会耗尽宿主的线粒体DNA，有些病毒，如人类免疫缺陷病毒，会劫持宿主的线粒体蛋白质，使其在宿主细胞内充分发挥作用。所有这些过程都涉及细胞蛋白、线粒体蛋白和病毒特异性蛋白的参与。本文就病毒利用细胞线粒体成功增殖和产生子代病毒的策略进行综述。
Mitochondria are multifunctional organelles with diverse roles including energy production and distribution, apoptosis, eliciting host immune response, and causing diseases and aging. Mitochondria-mediated immune responses might be an evolutionary adaptation by which mitochondria might have prevented the entry of invading microorganisms thus establishing them as an integral part of the cell. This makes them a target for all the invading pathogens including viruses. Viruses either induce or inhibit various mitochondrial processes in a highly specific manner so that they can replicate and produce progeny. Some viruses encode the Bcl2 homologues to counter the proapoptotic functions of the cellular and mitochondrial proteins. Others modulate the permeability transition pore and either prevent or induce the release of the apoptotic proteins from the mitochondria. Viruses like Herpes simplex virus 1 deplete the host mitochondrial DNA and some, like human immunodeficiency virus, hijack the host mitochondrial proteins to function fully inside the host cell. All these processes involve the participation of cellular proteins, mitochondrial proteins, and virus specific proteins. This review will summarize the strategies employed by viruses to utilize cellular mitochondria for successful multiplication and production of progeny virus.