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J. Biol. Chem., Vol. 282, Issue 19, 14608-14615, May 11, 2007

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Human T-cell Lymphotrophic Virus Type I Rex and p30 Interactions Govern the Switch between Virus Latency and Replication^*

Uma Sinha-Datta, Abhik Datta, Sofiane Ghorbel, Madeleine Duc Dodon, and Christophe Nicot¹

From the Department of Microbiology, Immunology, and Molecular Genetics, University of Kansas Medical Center, Kansas City, Kansas 66160 and Virologie Humaine, INSERM U758, Ecole Normale Supérieure de Lyon, IFR 128 Biosciences Lyon-Gerland, 46 allée d'ltalie, 69364 Lyon Cedex 07, France

Human T-cell lymphotrophic virus type I Rex and p30 are both RNA binding regulatory proteins. Rex is a protein that interacts with a responsive element and stimulates nuclear export of incompletely spliced viral RNAs thereby increasing production of virus particles. In contrast, p30 is involved in the nuclear retention of the tax/rex mRNA leading to inhibition of virus expression and possible establishment of viral latency. How these two proteins, with apparent opposite functions, integrate in the viral replication cycle is unknown. Here, we demonstrate that Rex and p30 form ribonucleoprotein ternary complexes onto specific viral mRNA. Our results explain the selective nuclear retention of tax/rex but not other viral mRNAs by p30. Whereas p30 suppresses Rex expression, it did not affect Rex-mediated nuclear export of RNA containing the Rex response element. In contrast, Rex was able to counteract p30-mediated suppression of viral expression and restore cytoplasmic tax/rex mRNA and Tax protein expression. Together, our data demonstrate a complex regulatory mechanism of antagonizing post-transcriptional regulators evolved by human T-cell lymphotrophic virus type I to allow a vigilant control of viral gene expression.

Received for publication, December 6, 2006 , and in revised form, March 13, 2007.

^* This work was supported by National Institutes of Health Grant AI058944 (to C. N.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Fig. S1C.

¹ To whom correspondence should be addressed: Dept. of Microbiology, Immunology, and Molecular Genetics, University of Kansas Medical Center, 3025 Wahl Hall West, 3901 Rainbow Blvd., Kansas City, KS 66160. Tel.: 913-588-6724; Fax: 913-588-7295; E-mail: cnicot{at}kumc.edu.

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