T cell effector functions are tightly regulated by their metabolism and to effectively eliminate pathogens, T cells rely on glycolysis to meet these energetic demands. However, during chronic viral infection, T cells progress towards an exhaustion program, characterized by impaired effector function, upregulation of inhibitory receptors, and dysfunctional metabolism states. Notably, exhausted T cells have impaired glucose uptake, decreased glycolysis and aerobic respiration, and shift toward fatty acid oxidation (FAO), leading to glucose deprivation and accumulation of reactive oxygen species (ROS). Despite current progress understanding exhaustion pathways, the key regulator(s) connecting metabolic dysfunction to T cell exhaustion remains poorly defined. Serine/threonine-protein phosphatase 6 regulatory subunit 3 (SAPS3) is a negative regulator of AMPK. Our lab recently found that SAPS3 is upregulated in exhausted CD8+ T cells compared with uninfected control, accompanied with lower levels of phosphorylated AMPK (pAMPK), showing that AMPK pathway activity is decreased in exhausted T cells. Therefore, we hypothesize that SAPS3 regulates T cell exhaustion by modulating T cell metabolism through AMPK signaling. To test this hypothesis, we generated T cell-specific SAPS3-deficient mice and infected them with Lymphocytic choriomeningitis virus (LCMV) Clone 13. Spleen and lymph nodes were harvested at day 8, 35, and 70 post-infection to characterize T cell exhaustion differentiation phenotypes and functional changes, while serum and peripheral organs were collected to assess viral burden. Compared to controls, SAPS3fl/fl CD4-Cre+ mice had a decrease in virus-specific CD8+ T cells, a reduction in TCF-1hi progenitor exhausted T cells, and a reduction in intermediate exhausted T cells, with a relatively increased distribution toward terminally exhausted T cells and elevated inhibitory receptor PD-1 and Tim-3 expression. These mice also showed higher viral titers in the peripheral organs, indicating impaired viral control. Together, our findings suggest that SAPS3 is intrinsically required in T cells to preserve stem-like pool and effector function during chronic viral infection.