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Journal of Virology, August 2000, p. 6866-6874, Vol. 74, No. 15
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Differences in the Ability of Human T-Cell Lymphotropic Virus Type 1 (HTLV-1) and HTLV-2 Tax To Inhibit p53 Function

Renaud Mahieux,1 Cynthia A. Pise-Masison,1 Paul F. Lambert,1 Christophe Nicot,2 Laura De Marchis,3 Antoine Gessain,4 Patrick Green,5 William Hall,6 and John N. Brady1,*

Laboratory of Receptor Biology and Gene Expression,1 Basic Research Laboratory, Section of Animal Models and Retroviral Infection,2 and Laboratory of Tumor Immunology and Biology,3National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892; Unité d'Oncologie Virale, Institut Pasteur, 75724 Paris, France4; Departments of Veterinary Biosciences and Molecular Virology, Immunology, and Medical Genetics, Center for Retrovirus Research and Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210-10935; and Department of Microbiology, University College, Dublin, Ireland6

Received 26 October 1999/Accepted 9 May 2000

We have analyzed the functional activity of the p53 tumor suppressor in human T-cell lymphotropic virus type 2 (HTLV-2)-transformed cells. Abundant levels of the p53 protein were detected in both HTLV-2A and -2B virus-infected cell lines. The p53 was functionally inactive, however, both in transient-transfection assays using a p53 reporter plasmid and in induction of p53-responsive genes in response to gamma irradiation. We further investigated HTLV-2A Tax and HTLV-2B Tax effects on p53 activity. Interestingly, although Tax-2A and -2B inactivate p53, the Tax-2A protein appears to inhibit p53 function less efficiently than either Tax-1 or Tax-2B. In transient-cotransfection assays, Tax-1 and Tax-2B inactivated p53 by 80%, while Tax2A reduced p53 activity by 20%. In addition, Tax-2A does not increase the steady-state level of cellular p53 as well as Tax-1 or -2B does in the same assays. Cotransfection assays demonstrated that Tax-2A could efficiently transactivate CREB-responsive promoters to the same level as Tax-1 and Tax-2B, indicating that the protein was functional. This report provides evidence of the first functional difference between the HTLV-2A and -2B subtypes. This comparison of the action of HTLV-1 and HTLV-2 Tax proteins on p53 function will provide important insights into the mechanism of HTLV transformation.

* Corresponding author. Mailing address: National Cancer Institute, Building 41/B201, NCI, NIH, Bethesda, MD 20892. Phone: (301) 496-0986. Fax: (301) 496-4951. E-mail: bradyj{at}exchange.nih.gov.

Journal of Virology, August 2000, p. 6866-6874, Vol. 74, No. 15
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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