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Journal of Virology, February 2009, p. 2048-2054, Vol. 83, No. 4
0022-538X/09/$08.00+0 doi:10.1128/JVI.01264-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Université du Québec à Montréal, Département des Sciences Biologiques, and Centre de recherche BioMed, Montréal (Québec) H2X 3X8, Canada,1 East Carolina University, Department of Microbiology and Immunology, Greenville, North Carolina 27834,2 Université Montpellier 1, Centre d'Études d'Agents Pathogènes et Biotechnologies pour la Santé (CPBS), CNRS/UM1/UM2 UMR 5236, Montpellier, France3
Received 18 June 2008/ Accepted 1 December 2008
Several studies have recently demonstrated the existence of human T-cell leukemia virus type 1 (HTLV-1) antisense transcripts, which allow the synthesis of the newly described HBZ protein. Although previous reports have been aimed at understanding the potential role of the HBZ protein in HTLV-1 pathogenesis, little is known as to how this viral gene is regulated. Here, using our K30-3'asLuc reporter construct, we show that the viral Tax protein upregulates antisense transcription through its action on the TRE sequences located in the 3' long terminal repeat. Generation of stable clones in 293T cells demonstrated that Tax-induced HBZ expression is importantly influenced by the integration site in the host genome. The cellular DNA context could thus affect the level of HBZ mRNA expression in infected cells.
Published ahead of print on 10 December 2008.
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