Identification of an initiator-like element within the HTLV-I promoter.

Using the 5' long terminal repeat (LTR) as its only promoter, the HTLV-1 provirus generates a single RNA transcript that undergoes differential splicing to express the various viral proteins. Examination of sequence near the transcription start site revealed an element resembling a transcriptional initiator (Inr) at position -8 to -15 in addition to the canonical TATA box at -25. To elucidate basal control of HTLV-I gene expression, functional traits of this element were examined. It specifically bound a protein complex, the mobility of which was altered by antibody to serum response factor, and independently mediated reporter gene expression. Mutating the Inr in a minimal construct reduced basal transcription, whereas mutation of the element within the context of the complete LTR left basal transcription unaffected. Presence of the element influenced transcription start site choices. Exhibiting many characteristics of an Inr, this element may play an important role in regulating HTLV-I gene expression in vivo, particularly during the long clinical latency period prior to development of HTLV-I-induced disease.