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Journal of Virology, October 2003, p. 11170-11179, Vol. 77, No. 20
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.20.11170-11179.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

T-Cell Receptor/CD28 Engagement When Combined with Prostaglandin E2 Treatment Leads to Potent Activation of Human T-Cell Leukemia Virus Type 1

Nancy Dumais,1,{dagger} Marie-Ève Paré,1 Simon Mercier,1 Salim Bounou,1 Susan J. Marriot,2 Benoit Barbeau,1* and Michel J. Tremblay1*

Centre de Recherche en Infectiologie, Hôpital CHUL, Centre Hospitalier Universitaire de Québec, and Département de Biologie Médicale, Faculté de Médecine, Université Laval, Québec, Canada G1V 4G2,1 Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 770302

Received 29 April 2003/ Accepted 29 June 2003

Infection with human T-cell leukemia virus type 1 (HTLV-1) is characterized by long latency periods, indicating that viral gene expression is under tight control. There is presently little information available regarding the nature of extracellular stimuli that can transactivate the regulatory elements of HTLV-1 (i.e., long terminal repeat [LTR]). To gain insight into the biological importance of externally induced activation pathways in virus gene expression, primary and established T cells were transfected with HTLV-1-based reporter gene vectors and then were treated with agents that cross-linked the T-cell receptor (TCR) or the costimulatory CD28 molecule with prostaglandin E2 (PGE2). We demonstrated that a potent induction of HTLV-1 LTR-driven reporter gene activity was seen only when the three agents were used in combination. Interestingly, similar observations were made when using C91/PL, a cell line that carries integrated HTLV-1 proviral DNA. This TCR-CD28-PGE2-mediated increase in virus transcription was dependent on protein kinase A activation and induction of the cAMP response element binding protein. Experiments with a mutated reporter construct further revealed the importance of the Tax-responsive elements in the HTLV-1 LTR in the observed up regulation of virus gene expression when TCR/CD28 engagement was combined with PGE2 treatment. The protein tyrosine kinases p56lck and the transmembrane tyrosine phosphatase CD45 were all found to be involved in TCR-CD28-PGE2-directed increase in HTLV-1 LTR activity. This study presents new information on the possible mechanisms underlying reactivation of this retrovirus.

* Corresponding author: Centre de Recherche en Infectiologie, RC709, Hôpital CHUL, Centre Hospitalier Universitaire de Québec, 2705 boul. Laurier, Québec (QC), Canada G1V 4G2. Phone: (418) 654-2705. Fax: (418) 654-2212. E-mail for Michael J. Tremblay: michel.j.tremblay{at}crchul.ulaval.ca. E-mail for Benoit Barbeau: benoit.barbeau{at}crchul.ulaval.ca.

{dagger} Present address: Département de Biologie, Faculté des Sciences, Université de Sherbrooke, Sherbrooke, Quebec, Canada J1K 2R1.

Journal of Virology, October 2003, p. 11170-11179, Vol. 77, No. 20
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.20.11170-11179.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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