1. [Adult T-cell leukemia induced by HTLV-1: before and after HBZ].
- Author
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Duc Dodon M, Mesnard JM, and Barbeau B
- Subjects
- Activating Transcription Factors metabolism, Animals, Basic-Leucine Zipper Transcription Factors genetics, Cell Division, Cyclic AMP Response Element-Binding Protein metabolism, Gene Products, tax metabolism, Genes, pX, Human T-lymphotropic virus 1 genetics, Human T-lymphotropic virus 1 pathogenicity, Humans, Leucine Zippers genetics, Leucine Zippers physiology, Leukemia-Lymphoma, Adult T-Cell genetics, Leukemia-Lymphoma, Adult T-Cell immunology, Models, Genetic, Promoter Regions, Genetic genetics, Proviruses genetics, RNA, Small Interfering pharmacology, Rabbits, Retroviridae Proteins, Terminal Repeat Sequences genetics, Transcription, Genetic drug effects, Transcription, Genetic genetics, Viral Proteins genetics, p300-CBP Transcription Factors metabolism, Basic-Leucine Zipper Transcription Factors physiology, Cell Transformation, Viral genetics, Gene Expression Regulation, Viral, Human T-lymphotropic virus 1 physiology, Leukemia-Lymphoma, Adult T-Cell virology, Viral Proteins physiology
- Abstract
Adult T-cell leukemia (ATL) is an often fatal leukemia of CD4+ T lymphocytes associated with a complex retrovirus, human T-cell leukemia virus type 1 (HTLV-1). Although the viral Tax protein is involved in the proliferation of infected cells during the preleukemic stages, Tax expression is not systematically detected in primary leukemic cells. In 2002, we described the characterization of a novel viral protein that we have termed HBZ for HTLV-1 bZIP factor. This viral factor is encoded on the antisense strand of HTLV-1 proviral DNA, demonstrating the existence of antisense transcription from a promoter located in the 3' LTR. HBZ can negatively control the expression of the other viral proteins by blocking the interaction between Tax and ATF/CREB factors and the recruitment of CBP/p300 by Tax on the promoter. Moreover, recent studies found that the viral HBZ gene was always expressed in leukemic cells, suggesting its involvement in the progression of the infected cells towards malignancy.
- Published
- 2010
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