The success of Chimeric Antigen Receptor (CAR) T-Cell therapy against non-solid malignancies has not been replicated in solid tumor settings. One contributing factor for the decreased efficacy could be due to the T-Cell expansion methodologies utilized for CAR transduced cells, which largely rely on generic proliferation techniques via the cross-linking of co-stimulatory receptors. These techniques result in the expansion of a T-cell population with mixed phenotype and polarization, which could result in poor trafficking to the tumor sites, poor effector function within the tumor environment and decreased persistence within the patient. The use of virus specific T-Cells (VSTs), which are naturally polarized to a Th1/Cytotoxic effector function, offer an alternative to improve CAR-T therapy against solid malignancies. Single cell RNASeq analysis of VSTs and conventional expanded T-Cells (ATCs), revealed an increase in transcripts associated with cytotoxic function, IL-12 signaling as well as mitochondrial respiration in VSTs. Phenotypic analysis demonstrated that VSTs are comprised mainly of effector and central memory cells, with a decreased proportion of regulatory, and naïve T-cell phenotypes. Examination of receptors associated with purinergic metabolism, showed a lower expression on VSTs compared to ATCs. Antigen stimulation of VSTs resulted in decreased secretion of Th2 and myeloid stimulating cytokines in contrast to higher amounts from ATC stimulation. Taken together, these results indicate the utility of VSTs as a viable platform for CAR-T therapy.