Analysis of a novel defective HTLV‐I provirus and detection of a new HTLV‐I‐induced cellular transcript

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Abstract
HTLV‐I generally integrates at least one full‐length copy in adult T‐cell leukemia (ATL) cells. A group of patients without full‐length provirus have a unique conserved truncation of the provirus which retains env‐pX‐3′LTR. Tumor cells of a patient from this group were genetically analyzed. Analysis of the 5′ and 3′ cellular flanking region adjacent to the provirus suggest that the defective provirus was integrated immediately downstream of a promoter of an unknown cellular gene. The activity of the promoter was weak but was responsive to Tax‐like HTLV‐I LTR. The provirus may have utilized it as a substitute for the 5′LTR and thus 3′LTR may have become an alternative promoter for the cellular gene, which may give similar viral‐cellular interactions to that of general cases with full‐length proviruses. Surprisingly, the 3′ cellular flanking region which is thought to be controlled originally by the promoter is constitutively expressed specifically in an HTLV‐I producing ATL cell line HUT102G, in which the corresponding region is not modified by provirus. The detection of this HTLV‐I‐induced transcript provides a probe to find an HTLV‐I inducible unknown cellular gene that may be related to the pathogenesis of ATL.