This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Despite a reduced incidence of HIV dementia in patients on highly active antiretroviral therapy (HAART), the improved survival has resulted in increased cumulative prevalence of nervous system complications of AIDS. Fundamental gaps remain in knowledge relating to mechanisms and pathways involved in the development of HIV-associated neurologic disease. Lesions associated with encephalitis include marked astrocytic and microglial activation with frequent multinucleated giant cells, high viral load and lesions consisting of multiple disseminated foci of inflammatory cells throughout the brain. The pathogenesis of the lesions is unknown, but it is thought to be associated with alterations in the BBB. Heretofore, it has not been possible to determine if an individual has encephalitis before post mortem examination. By determining levels of the glial protein S100b in serum, we show that it is possible not only to determine correlates post mortem, but also to predict which individuals will have encephalitis before death. This could have profound impact on elucidating the pathogenesis of neuroAIDS using the rhesus macaque model allowing one to euthanize an animal during the earliest stages of neurological disease or to predict HIVE in patients infected with HIV and thus, tailor treatment administered.
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