The human T-cell leukemia virus type I (HTLV-I) promoter, found within the 5’ long terminal repeat (LTR) of the provirus, is approximately 350 base pairs in length.  Multiple DNA elements in the viral promoter have been shown to bind a variety of cellular transcription factors including CREB, ATF, Ets, and Sp1.  These proteins regulate viral gene expression in several ways.  Basal transcription, which occurs immediately following infection or after a period of latency, requires a specific subset of cellular regulators.  Binding of these factors to the LTR initiates early rounds of basal transcription resulting in production of the viral transactivator Tax, an activator of both viral and cellular gene expression.  Although Tax does not bind DNA directly, it is recruited to the LTR through interactions with one or more cellular transcription factors.  Because of its ability to increase the DNA binding affinity of certain transcription factors and recruit the coactivators CBP/p300 and P/CAF to the LTR, Tax may alter the composition of cellular protein complexes associated with the viral promoter causing a switch from basal to activated transcription.  The modular control of HTLV-I transcription is regulated by diverse cellular factors as well as by Tax, and this regulation may contribute to disease progression associated with this virus.  This review will discuss transcriptional regulation of the HTLV-I LTR; focusing on regulatory DNA elements in the LTR, specific cellular factors that regulate the LTR, and mechanisms of Tax activation of viral gene expression.