Abstract
Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL) and is also associated with a variety of lymphocyte-mediated diseases. The HTLV-1 basic leucine zipper (HBZ) gene, found to be consistently expressed in ATL, has recently been the subject of intensive research efforts. In this review, we summarize recent findings about HBZ and discuss its roles and functions not only in the virus life cycle, but also in HTLV-1 disease pathogenesis.
Highlights
Adult T-cell leukemia/lymphoma (ATL) was proposed as a distinct clinical entity in 1975 by Takatsuki et al [1]
Human T-cell leukemia virus type 1 (HTLV-1) was discovered in 1980 as the cause of ATL and was the first retrovirus associated with a disease in humans [2,3]
Expression of the human T-cell leukemia virus type 1 (HTLV-1) bZIP factor gene (HBZ), an antisense mRNA transcribed from the 3' LTR, has been shown to be consistently expressed in ATL cells [5]; HBZ may have a functional role in cellular transformation and leukemogenesis
Summary
Adult T-cell leukemia/lymphoma (ATL) was proposed as a distinct clinical entity in 1975 by Takatsuki et al [1]. In contrast to JunB and c-Jun, the interaction of HBZ with JunD stimulates its transcriptional activity and results in the activation of JunD-dependent cellular genes including human telomerase reverse transcriptase (hTERT) [33] The significance of this finding is that the activation of telomerase is a critical late event in tumor progression and that HBZ is the only viral protein expressed in all ATL cells. Introduction of mutations that either abrogated HBZ protein expression or disrupted the HBZ mRNA without affecting the protein coding sequence indicated that the HBZ RNA, a stem loop structure near the amino terminus of the gene, promoted T-cell proliferation; this contrasts with the finding that the HBZ protein inhibited Tax-mediated transactivation [5] These findings led to the conclusion that the HBZ gene has a bimodal function in two different molecular forms. Some aspects of the HTLV-1 antisense transcript function may be conserved in other retroviruses since similar antisense RNAs have been reported for HIV-1 [41]
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