Apoptosis prevention as a mechanism of immune evasion.
When cells are infected with viruses, they may trigger their apoptosis programs. In unicellular organisms, this may have protected cell populations by limiting viral replication from infected cells. Multicellular organisms can also trigger the apoptosis program after viral infection. In response, viruses have evolved a wide variety of inhibitors of apoptosis. In higher organisms, the outcome of viral infections is largely determined by the immune system. Since apoptosis is intimately linked to the function and regulation of the immune system, the ability of viruses to inhibit apoptosis could profoundly alter the immune response. Viral antiapoptotic proteins could protect infected cells from apoptosis induced by cytotoxic lymphocytes, alter antigen cross-presentation and the priming of the immune response, or modulate the expression of danger signals from sites of infection. The virus/host interaction is likely to provide useful lessons regarding the workings of the mammalian immune system.
Aubert
Martine
M
Program in Infectious Diseases, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N., Seattle, WA 98125, USA.
Jerome
Keith R
KR
D000818:Animals; D017209:Apoptosis / Q000276:immunology*; D006790:Host-Parasite Interactions; D014777:Virus Diseases / Q000276:immunology* / Q000473:pathology; D018406:Virus Physiological Phenomena