To kill or be killed: viral evasion of apoptosis.
In the struggle between virus and host, control over the cell's death machinery is crucial for survival. Viruses are obligatory intracellular parasites and, as such, must modulate apoptotic pathways to control the lifespan of their host in order to complete their replication cycle. Many of the counter-assaults mounted by the immune system incorporate activation of the apoptotic pathway-particularly by members of the tumor necrosis factor cytokine family-as a mechanism to restrict viral replication. Thus, apoptosis serves as a powerful selective pressure for the virus to evade. However, for the host, success is harsh and potentially costly, as apoptosis often contributes to pathogenesis. Here we examine some of the molecular mechanisms by which viruses manipulate the apoptotic machinery to their advantage and how we (as vertebrates) have evolved and learned to cope with viral evasion.
Benedict
Chris A
CA
Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.
Norris
Paula S
PS
Ware
Carl F
CF
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D003546:Cysteine Endopeptidases / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D006801:Humans; D007372:Interferons / Q000502:physiology; D051379:Mice; D008954:Models, Biological; D018716:Molecular Mimicry; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor / Q000502:physiology; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D014714:Vertebrates / Q000276:immunology / Q000821:virology; D014777:Virus Diseases / Q000276:immunology / Q000473:pathology / Q000821:virology*; D018406:Virus Physiological Phenomena; D014779:Virus Replication
D016207:Cytokines; D019253:Proto-Oncogene Proteins c-bcl-2; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D007372:Interferons; D003546:Cysteine Endopeptidases