Viral control of mitochondrial apoptosis

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 reac...

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Bibliographic Details
Published in:PLoS pathogens 2008-05, Vol.4 (5), p.e1000018-e1000018
Main Authors: Galluzzi, Lorenzo, Brenner, Catherine, Morselli, Eugenia, Touat, Zahia, Kroemer, Guido
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Biochemistry/Cell Signaling and Trafficking Structures
Biochemistry/Chemical Biology of the Cell
Biochemistry/Transcription and Translation
Cancer
Cell Biology
Host-Pathogen Interactions
Immune system
Infectious Diseases
Infectious Diseases/HIV Infection and AIDS
Influence
Mitochondria
Mitochondria - pathology
Mitochondria - virology
Mitochondrial Membranes - physiology
Molecular Biology
Permeability
Physiological aspects
Proteins
Proto-Oncogene Proteins c-bcl-2 - physiology
Review
Viral infections
Viral proteins
Viral Proteins - physiology
Virus Diseases - metabolism
Virus Diseases - pathology
Virus Physiological Phenomena
Viruses
Viruses - pathogenicity
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Summary: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.
ISSN:1553-7374
1553-7366
1553-7374
DOI:10.1371/journal.ppat.1000018