ALCOHOL AND SIV ENCEPHALITIS: PBMC CHEMOTAXIS MODULATION FOLLOWING INFECTION

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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. Simian Immunodeficiency virus (SIV) infection of macaques is an important animal model for the acquired immunodeficiency syndrome (AIDS) that recapitulates most features of HIV infection, including CNS disease. Alcohol has been shown to exacerbate neurological diseases in humans, and it is known that there is a higher incidence of HIV infection among chronic alcohol abusers. However, it is not known if this translates into a higher incidence of neurological complications associated with HIV infection. Numbers of SIV infected PBMCs found within the brain of monkeys with terminal AIDS correlates with severity of disease. To examine if chronic alcohol abuse leads to increased PBMC migration into the CNS following SIV infection we determined chemotactic indices. These were obtained by measuring the ability of PBMCs freshly obtained from macaques to migrate in a directed manner to CCLs 3,4 &7 before and after SIV infection. The results showed that there is an increase in migration of PBMCs towards CCLs 3, 4 & 7 following SIV infection in a CCR5 dependent manner and that this is exacerbated by chronic alcohol administration.