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. A leading theory for the pathogenesis of neuroAIDS is that a specific bone marrow derived blood monocyte is infected with HIV, becomes activated, then traffics into the CNS where it becomes a perivascular macrophage and sets off a cascade of events that result in neuronal injury. While there is strong evidence supporting the key role of infected and/or activated monocytic phagocytes (MPs) in neuroAIDS pathogenesis, there is little information on the dynamics of MP trafficking, MP turnover in the CNS and neuronal recovery. In this project, we are using an accelerated model of SIV encephalitis to investigate macrophage trafficking in the CNS and the role of macrophages in HIV/SIV neuroinvasion.
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