Viral control of mitochondrial apoptosis

被引:358
作者
Galluzzi, Lorenzo [1 ,2 ,3 ]
Brenner, Catherine [4 ]
Morselli, Eugenia [1 ,2 ,3 ]
Touat, Zahia [4 ]
Kroemer, Guido [1 ,2 ,3 ]
机构
[1] INSERM, U848, Villejuif, France
[2] Inst Gustave Roussy, Villejuif, France
[3] Univ Paris 11, Fac Med, Villejuif, France
[4] Univ Versailles St Quentin, PRES UniverSud Paris, CNRS, UMR8159, Versailles, France
关键词
D O I
10.1371/journal.ppat.1000018
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Throughout the process of pathogen-host co-evolution, viruses have developed a battery of distinct strategies to overcome biochemical and immunological defenses of the host. Thus, viruses have acquired the capacity to subvert host cell apoptosis, control inflammatory responses, and evade immune reactions. Since the elimination of infected cells via programmed cell death is one of the most ancestral defense mechanisms against infection, disabling host cell apoptosis might represent an almost obligate step in the viral life cycle. Conversely, viruses may take advantage of stimulating apoptosis, either to kill uninfected cells from the immune system, or to induce the breakdown of infected cells, thereby favoring viral dissemination. Several viral polypeptides are homologs of host-derived apoptosis regulatory proteins, such as members of the Bcl-2 family. Moreover, viral factors with no homology to host proteins specifically target key components of the apoptotic machinery. Here, we summarize the current knowledge on the viral modulation of mitochondrial apoptosis, by focusing in particular on the mechanisms by which viral proteins control the host cell death apparatus.
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页数:19
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