Avoiding the kiss of death: how HIV and other chronic viruses survive.
Virus-specific CD8 T cells during chronic infection often exceed in numbers virus-replicating infected cells. Why then do antiviral CD8 T cells not do a better job of controlling infection? Although viral strategies for immune evasion are well known, this review will focus on changes in the CD8 T cell that interfere with cytolytic function. Most antiviral CD8 T cells in chronic infection do not express perforin, a molecule that is required for cytolysis. IL-2 and other costimulatory signals can restore cytotoxicity that has been impaired, suggesting a role for CD4 T cell anergy. The chance to eradicate an infection by T cell mediated lysis is undermined after an infection becomes established, in part because the effector immune response is impaired in the setting of chronic antigen.
Lieberman
Judy
J
Center for Blood Research and Department of Pediatrics, Harvard Medical School, 800 Huntington Avenue, Boston, MA 02115, USA. lieberman@cbr.med.harvard.edu
Manjunath
N
N
Shankar
Premlata
P
D000818:Animals; D002454:Cell Differentiation; D002908:Chronic Disease; D017635:Clonal Anergy; D004195:Disease Models, Animal; D015658:HIV Infections / Q000276:immunology*; D006801:Humans; D008562:Membrane Glycoproteins / Q000502:physiology; D051379:Mice; D018448:Models, Immunological; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins; D016097:Simian Acquired Immunodeficiency Syndrome / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D014777:Virus Diseases / Q000276:immunology*; D014780:Viruses / Q000472:pathogenicity*
D008562:Membrane Glycoproteins; D052899:Pore Forming Cytotoxic Proteins; D054353:Perforin