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Experimental Microbial Dysbiosis Does Not Accelerate Disease Progression in SIV Infection

HIV-1 infection is associated with inflammation that is not fully reversed with antiretroviral therapy. Inflammation in HIV-infected individuals is associated with enrichment of disease-associated intestinal microflora, namely, Proteobacteria. Although several studies have indicated that therapeutic administration of probiotic species has immunological benefit, an empirical assessment of the contribution of microbial dysbiosis to disease progression is lacking. To assess the contribution of bacterial GI tract dysbiosis to lentiviral disease progression, we administered the antibiotic vancomycin to macaques pre- and post-SIV-infection. Vancomycin treatment resulted in a significant and progressive increase in the relative frequency of fecal Proteobacteria and decrease of Firmicutes during chronic SIV infection. Surprisingly, no adverse differences in viremia, immune activation, nor other canonical indicators of disease progression were observed in experimental animals throughout SIV-infection. Our results demonstrate that key features of HIV-associated inestinal dysbiosis are ancillary to disease progression in a non-human primate model of HIV-1 disease progression.

Jason Brenchley

Jason Brenchley is a Senior Investigator of the Barrier Immunity section in the Laboratory of Viral Diseases, NIAID, NIH. He did his undergraduate work at the Idaho State University and his PhD at the University of Texas Southwestern Medical Center. After completing post doctoral work at the VRC, NIAID, he became a tenure track investigator in NIAID, NIH. His laboratory aims to understand the mechanisms underlying disease progression in HIV-infected individuals using a primate model. In particular, the barrier immunity section aims to understand how pathology within the structural and immunological barrier of the GI tract leads to systemic microbial translocation and inflammation and how long-term antiretroviral therapy reverses these. The overarching goal is to develop novel therapeutic interventions to improve the physiology of the GI tract in HIV-infected individuals. The laboratory is also interested in understanding the mechanisms responsible for the nonprogressive nature of SIV infection in its natural African nonhuman primate hosts. They have found that African green monkeys down-regulate expression of CD4 as naïve CD4 T cells become immunologically experienced. This CD4 down regulation renders the cells

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