Brain Regional Dependence of Antiviral and Inflammatory Genes Following Simian Immunodeficiency Virus Infection and Antiretroviral Therapy

Abstract Human immunodeficiency virus (HIV) initiates a perpetual cycle of inflammation in the brain that results neuronal damage and consequent neurologic dysfunction. Since HIV preferentially infects damages specific regions, there is need for study antiviral immune markers region manner. We have evaluated expression (IFNa, IFNb, TRAIL, MX1) (CCL2, IL-6, IL-1b, IL-10) across nine regions our virally suppressed rhesus macaque model simian (SIV) infection. Rhesus macaques from four groups (uninfected, SIV, SIV/ART, SIV/ART cessation) were perfused, obtained by region, snap frozen liquid nitrogen. RNA was extracted qRT-PCR performed to quantify genes interest each region. Antiviral (MX1, TRAIL) expressed all equally groups, with occasional increase MX1 SIV infected animals. Alternatively, common (IL-6, CCL2) not any group, excepting thalamus. Other (IFN-a) (IL-10) consistently uninfected However, effects ART on these other pertinent (IFN-b, IL-1b) dependent. Altogether, data suggest marker dynamic differs depending under investigation. This knowledge has implications way are studied implies Supported grants NIH (5R01DA052859-02) funded Johns Hopkins University Center AIDS Research (P30AI094189-01A1)