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Cited by 73

The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.

Human T-Cell Leukemia Virus Type 1 (HTLV-1) bZIP Factor Requires Cellular Transcription Factor JunD To Upregulate HTLV-1 Antisense Transcription from the 3′ Long Terminal Repeat

Gazon, Hélène, Lemasson, Isabelle, Polakowski, Nicholas, Césaire, Raymond, Matsuoka, Masao, Barbeau, Benoit, Mesnard, Jean-Michel, Peloponese, Jean-Marie·2012·Journal of Virology
DOI 10.1128/jvi.00661-12
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Abstract

Infection with the human T-cell leukemia virus type 1 (HTLV-1) results in a variety of diseases including adult T-cell leukemia (ATL), a fatal malignancy characterized by the uncontrolled proliferation of virally infected CD4 + T cells. The HTLV-1 basic leucine zipper factor (HBZ) is believed to contribute to development and maintenance of ATL. Unlike the other HTLV-1 genes, the hbz gene is encoded on the complementary strand of the provirus and therefore is not under direct control of the promoter within the 5′ long terminal repeat (LTR) of the provirus. This promoter can undergo inactivating genetic or epigenetic changes during the course of ATL that eliminates expression of all viral genes except that of hbz . In contrast, repressive modifications are not known to occur on the hbz promoter located in the 3′ LTR, and hbz expression has been consistently detected in all ATL patient samples. Although Sp1 regulates basal transcription from the HBZ promoter, other factors that activate transcription remain undefined. In this study, we used a proviral reporter construct deleted of the 5′ LTR to show that HBZ upregulates its own expression through cooperation with JunD. Activation of antisense transcription was apparent in serum-deprived cells in which the level of JunD was elevated, and elimination of JunD expression by gene knockout or shRNA-mediated knockdown abrogated this effect. Activation through HBZ and JunD additionally required Sp1 binding at the hbz promoter. These data favor a model in which JunD is recruited to the promoter through Sp1, where it heterodimerizes with HBZ thereby enhancing its activity. Separately, hbz gene expression led to an increase in JunD abundance, and this effect correlated with emergence of features of transformed cells in immortalized fibroblasts. Overall, our results suggest that JunD represents a novel therapeutic target for the treatment of ATL.

Overview

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Crossref · 10.1128/jvi.00661-12

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Metadata

Authors
Gazon, H., Lemasson, I., Polakowski, N., Césaire, R., Matsuoka, M., Barbeau, B., Mesnard, J.-M., & Peloponese, J.-M.
Affiliations
  • CPBS, CNRS UMR 5236, Montpellier, France
  • East Carolina University, Department of Microbiology and Immunology, Greenville, North Carolina, USA
  • Laboratoire de Virologie-Immunologie JE2503, Centre Hospitalier et Universitaire de Fort de France, Fort de France, Martinique, France
  • Laboratory of Virus Control, Institute for Virus Research, Kyoto University, Kyoto, Japan
  • Université du Québec à Montréal, Département des Sciences Biologiques, Montréal, Québec, Canada
Venue
Journal of Virology
Publisher
American Society for Microbiology
Published
2012-09
Volume
86
Issue
17
Pages
9070-9078
ISSN
  • 0022-538X
  • 1098-5514
DOI
10.1128/jvi.00661-12
Cited by
73
References
65
Language
en
Licence
journals.asm.org/non-commercial-tdm-license (tdm)

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.