The immune system has been observed to mobilize cytotoxic T lymphocyte (CTL) and neutralizing antibody titers to HIVinfection. Initially, these responses are not strong or broad enough to control HIV infection. Triple combination antiretroviral therapy serves to reduce viral proliferation rates, while producing a downregulation of vital immune responses by reducing their antigen stimulation. New observations in patients who are non-adherent to triple combination antiretroviral therapy over a period of several months to a year show that low-level exposure to virus can boost a robust enough immune system to keep viral proliferation at nearly undetectable levels in the complete abscence of therapy. This phenomenon can be described as 'auto-vaccination'. If HIV infection is to be eradicated, this type of immune activation needs to be mobilized in the presence of triple combination antiretroviral therapy. Efficiently stimulating the immune response however, is not well understood. This study will serve to characterize the virus exposure necessary to moblize the immune system and quantitate the minimal CTL and antibody levels necessary to reproduce the HIV control observed in the cohort studied. Further, analysis will be performed on the cytokine and molecular signalling used in mounting such a response. The latter will identify possible genes/gene products which may be used to augment immune response in patients, speeding up the 'auto vaccination' and reducing the risk of viral escape.
