Abstract The production of IL-21 by CD4 T cells is one mechanism by which CD8 T cells can sustain their effector functions, including increased metabolic demand, during chronic viral infection. However, signaling cascades downstream of IL-21 that control effector function in CD8 T cells remain incompletely understood. One such set of targets are the PIM kinases. This family of serine/threonine kinases functions downstream of IL-21 via JAK-STAT signaling and are involved in diverse cellular processes. Treatment of activated CD8 T cells with IL-21 induces expression of PIM1 kinase and phosphorylation of its targets S6 T372, 4EBP T37/42, and BAD S112, which promote transcription and inhibit apoptosis. Using the lymphocytic choriomeningitis virus (LCMV) Clone 13 mouse model of chronic infection, we show that virus-specific effector CD8 T cells display the highest expression of Pim1compared to exhausted and progenitor CD8 T cells at day 21 post-infection (p.i.). Infection of Pim1−/−mice with LCMV Clone 13 results in reduced virus-specific effector CD8 T cells and increased exhausted CD8 T cells at days 21–23 p.i. compared to wildtype controls. In addition, pharmacological inhibition of PIM kinases with AZD1208, a pan-PIM kinase inhibitor, in activated CD8 T cells results in compromised mitochondrial metabolism, which is essential for effector CD8 T cell function. Overall, our results suggest that PIM kinases are critical for effector CD8 T cell differentiation, function, and metabolism in the control of chronic viral infection. Supported by grants from NIH (R01 AI148403) and by an award from the Medical College of Wisconsin Center for Immunology.