From sabotage to camouflage: viral evasion of cytotoxic T lymphocyte and natural killer cell-mediated immunity.
The outcome of a virus infection is strongly influenced by interactions between host immune defences and virus 'antidefence' mechanisms. For many viruses, their continued survival depends on the speed of their attack:their capacity to replicate and transmit to uninfected hosts prior to their elimination by an effective immune response. In contrast, the success of persistent viruses lies in their capacity for immunological subterfuge: the evasion of host defence mechanism by either mutation (covered elsewhere in this issue, by Gould and Bangham, pp. 331-338) or interference with the action of host cellular proteins that are important components of the immune response. This review will focus on the strategies employed by persistent viruses against two formidable host defences against virus infection: the CD8+ cytotoxic T lymphocyte (CTL) and natural killer (NK) cell responses.
Department of Microbiology, the University of Western Australia, Western Australia, Australia.
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Davis-Poynter
D000818:Animals; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular; D007694:Killer Cells, Natural / Q000276:immunology*; D018448:Models, Immunological; D014777:Virus Diseases / Q000276:immunology; D014780:Viruses / Q000276:immunology*