Cellular immune response to human immunodeficiency virus

Citation
Pj. Norris et Es. Rosenberg, Cellular immune response to human immunodeficiency virus, AIDS, 15, 2001, pp. S16-S21
Citations number
31
Categorie Soggetti
Immunology
Journal title
AIDS
ISSN journal
02699370 → ACNP
Volume
15
Year of publication
2001
Supplement
2
Pages
S16 - S21
Database
ISI
SICI code
0269-9370(200102)15:<S16:CIRTHI>2.0.ZU;2-V
Abstract
Despite recent success with the use of highly active antiretroviral therapy , eradication of HIV type 1 appears beyond the capabilities of presently av ailable therapy. Therefore, greater emphasis has been given to finding mech anisms that promote immunologic control of viral replication rather than er adication. Although the correlates of immune protection in HIV-1 infection remain undefined, increasing evidence indicates that HIV-1-specific cellula r immune responses may play a critical role in antiviral control. Vigorous HIV-1-specific CD4+ T-helper cell and CD8+ cytotoxic T-lymphocyte responses may play a critical role in control of viral replication in the absence of antiretroviral therapy, which has been demonstrated in individuals with lo ng-term nonprogressive infection. However, in chronic, progressive HIV-1 in fection, virus-specific T-helper cell responses are typically weak or absen t in all stages of disease, and HIV-1-specific cytotoxic T-lymphocyte respo nses wane over time, presumably due to the lack of HIV-1-specific T helper cells. Effective treatment of individuals during acute HIV-1 seroconversion syndrome appears to restore HIV-1-specific T-helper cell responses, which are otherwise only observed in persons with long-term nonprogressive infect ion. This observation, along with anecdotal reports of individuals successf ully controlling viral replication after treating acute HIV-1 infection, pr ovides immunologic rationale for structured treatment interruption and othe r immunotherapeutic approaches designed to augment HIV-1-specific immune re sponses. (C) 2001 Lippincott Williams & Wilkins.