During HIV-1 infection, the importance of CD8+ T cells have been well established to play a key role in control of viremia, where emergence of HIV-specific CD8+T cells are associated with rapid decrease of viral load. However, despite the appearance of HIV-1-specific CD8+ T cell responses and in some cases control of viremia, HIV-1 is not successfully eliminated from HIV-1-infected individuals. The underlying mechanisms for this are not completely understood, but T cell dysfunction and chronic immune activation are frequently regarded to be contributing factors. CD96, also called T cell ACT ivating I ncreased L ate E xpression (TACTILE), is expressed by both T cells and NK cells and is a member of a group of IgG superfamily receptors that bind nectins and nectin-like proteins. CD96 is associated with NK and T cell effector functions and it has been shown that engagement of CD96 on NK cells enhances cytotoxicity. However, its function on T cells remains undetermined. This study will investigate the regulation and function of CD96 as well as examine CD96 expression during the course of HIV-1 infection where altered expression of this molecule could result in suboptimal T cell responses. Findings of this study may provide a potential contributing cause for HIV-1 related pathogenesis and will provide novel insight to improve our understanding of the consequences of chronic immune activation.