Cellular immune response to human immunodeficiency virus.

Despite recent success with the use of highly active antiretroviral therapy, eradication of HIV type 1 appears beyond the capabilities of presently available therapy. Therefore, greater emphasis has been given to finding mechanisms that promote immunologic control of viral replication rather than eradication. Although the correlates of immune protection in HIV-1 infection remain undefined, increasing evidence indicates that HIV-1-specific cellular 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 long-term nonprogressive infection. However, in chronic, progressive HIV-1 infection, virus-specific T-helper cell responses are typically weak or absent in all stages of disease, and HIV-1-specific cytotoxic T-lymphocyte responses 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 infection. This observation, along with anecdotal reports of individuals successfully controlling viral replication after treating acute HIV-1 infection, provides immunologic rationale for structured treatment interruption and other immunotherapeutic approaches designed to augment HIV-1-specific immune responses.