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Santiago and Wilson labs frame the gene expression landscape of HIV-1 infected gut T cells exposed to enteric bacteria

Counteracting HIV-1 and its comorbidities would require a deeper understanding of how HIV-1 alters its target cells in critical tissue compartments. The gastrointestinal (GI) tract is a major site of early HIV-1 replication and death of CD4+ T cells. As HIV-1 replicates in the gut, the protective epithelial barrier gets disrupted, causing the entry of bacteria into the underlying tissue and the bloodstream, leading to inflammation and clinical complications even in HIV-1-infected patients taking antiviral drugs. Counteracting these pathogenic processes may require in-depth understanding of the molecular pathways that HIV-1 and microbes utilize to infect, functionally alter and/or kill CD4+ T cells. However, to date, the nature of the genes altered by relevant transmitted/founder HIV-1 strains and gut bacteria in intestinal CD4+ T cells remains unknown.
 Reporting in PLOS Pathogens (published online February 27, 2017), Yoder et al. now provide the first gene expression profiles of primary gut CD4+ T cells infected in cell culture with transmitted/founder HIV-1 in the context of microbes found in the GI tract of HIV-1 infected patients. Their findings reveal common and distinct signaling pathways altered by HIV-1 depending on the presence of microbes that may shed light on infection, inflammation and CD4+ T cell depletion in HIV-1 infected individuals. These altered pathways may be critical in efforts to curb chronic inflammation in HIV-1 infected individuals and provide novel targets for curative strategies.
 The study was supported by the National Institutes of Health AI108404 (Wilson), R56 AI116271 (Santiago/Wilson), The University of Colorado RNA Bioscience Initiative (Santiago/Wilson), the Department of Medicine Early Career Scholar Program (Santiago). Co-authors include CU School of Medicine researchers Alyson Yoder, Kejun Guo, Stephanie Dillon, Tzu Phang, Eric Lee, Michael Harper, Karen Helm and Martin McCarter.