Viral control of mitochondrial apoptosis. Review uri icon

Overview

abstract

  • 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.

publication date

  • May 30, 2008

Research

keywords

  • Apoptosis
  • Mitochondria
  • Viral Proteins
  • Virus Physiological Phenomena
  • Viruses

Identity

PubMed Central ID

  • PMC2376094

Scopus Document Identifier

  • 44949151607

Digital Object Identifier (DOI)

  • 10.1371/journal.ppat.1000018

PubMed ID

  • 18516228

Additional Document Info

volume

  • 4

issue

  • 5