This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Major Hypotheses: Immunologic, virologic, and host factors data obtained at baseline will be able to predict subsequent rates of clinical and immunologic progression after antiretroviral (ART) cessation. Specifically, the investigators hypothesize that the following factors will be associated with: More rapid progression: -lower CD4+ nadir, CD4+ gain on ART, higher levels of immune activation (CD8+/CD38+T-cells), lower levels of thymic proliferative capacity (TREC), higher IL-7 levels, decreased IGF-I levels, and older age. -the presence of certain MHC class I HLA alleles (certain B*35 subtypes and B*5301) and homozygosity of the HLA class I loci. -higher pre-ART and post cessation viral setpoint. Slower progression: HLA class I loci: -HLA-B27, B57, and B51. The rate of illness will be low (<10% per year). Secondary Hypotheses: -ART cessation will result in improved quality of life, lower lipid and glucose levels, and improved body habitus; and resumption of ART will result in worsening of these parameters. -ART cessation will reduce health care resource utilization and resumption of ART will result in increased utilization. -Plasma viral rebound after ART cessation will result in cognitive dysfunction due to simultaneous high CSF viral burdens. -In patients who resume ART, the early virologic response will predict the subsequent virologic response.
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