Human immunodeficiency virus HIV is characterized by profound loss of CD4T cells particularly in the gastrointestinal tract, chronic immune activation, and evidence of translocation of microbial products from the gut. Along with the loss of CD4 T cells, IL-17-producing CD4 T cells known as Th17 cells are also lost during HIV infection and fail to recover during the course of disease. Th17 cells are an important component of the mucosal immune system as they help maintain the intestinal epithelial barrier and protect against mucosal pathogens. The loss of Th17 cells likely contributes to increased translocation of microbial products and chronic immune activation during HIV infection. Why Th17 cells do not recover during infection is not known. We hypothesized that the failure of Th17 cells to recover during HIV infection is due to the dysregulation of the signaling pathways essential for the generation of Th17 responses. Using the simian immunodeficiency virus SIV model, we sought to determine if the Th17 differentiation and transcriptional pathways were altered during infection.