Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus and the causative infectious agent of both HAM/TSP, a chronic inflammatory disease of the central nervous system, and ATL, an aggressive and fatal disease of CD4+ T-cells. HTLV-1-associated disease development occurs after an extensive clinical latency period upwards of several decades and lacks ideal therapeutic strategies. Not only is prognosis poor, but the molecular mechanism(s) behind disease development are not greatly understood. My lab utilizes molecular tools, coupled with both in vitro and in vivo models of infection and disease, to understand the cellular and viral players involved in genetic and epigenetic regulation of HTLV-1 gene expression and oncogenesis.