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J. Biol. Chem., Vol. 279, Issue 10, 9208-9214, March 5, 2004

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Inhibition of HIV-1 Replication by Cell-penetrating Peptides Binding Rev^*

Armelle Roisin, Jean-Philippe Robin, Nathalie Dereuddre-Bosquet, Anne-Laure Vitte, Dominique Dormont¶, Pascal Clayette, and Pierre Jalinot||

From the Laboratoire de Biologie Moléculaire de la Cellule, UMR5161, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, 46, Allée d'Italie, 69364 Lyon Cedex 07, France, Société de Pharmacologie et d'Immunologie-BIO, c/o Service de Neurovirologie, Commissariat à l'Energie Atomique (CEA), Direction des Sciences du Vivant/Département de Recherche Médicale (DSV/DRM), Centre de Recherche du Service de Santé des Armées (CRSSA), Ecole Pratique de Hautes Etudes (EPHE), Université Paris XI, 18, route du Panorama, B. P. 6, 92265 Fontenay aux Roses, France, and ^¶Service de Neurovirologie, CEA, DSV/DRM, CRSSA, EPHE, Université Paris XI, 18, route du Panorama, B. P. 6, 92265 Fontenay aux Roses, France

New therapeutic agents able to block HIV-1 replication are eagerly sought after to increase the possibilities of treatment of resistant viral strains. In this report, we describe a rational strategy to identify small peptide sequences owning the dual property of penetrating within lymphocytes and of binding to a protein target. Such sequences were identified for two important HIV-1 regulatory proteins, Tat and Rev. Their association to a stabilizing domain consisting of human small ubiquitin-related modifier-1 (SUMO-1) allowed the generation of small proteins named SUMO-1 heptapeptide protein transduction domain for binding Tat (SHPT) and SUMO-1 heptapeptide protein transduction domain for binding Rev (SHPR), which are stable and efficiently penetrate within primary lymphocytes. Analysis of the antiviral activity of these proteins showed that one SHPR is active in both primary lymphocytes and macrophages, whereas one SHPT is active only in the latter cells. These proteins may represent prototypes of new therapeutic agents targeting the crucial functions exerted by both viral regulatory factors.

Received for publication, October 22, 2003 , and in revised form, December 5, 2003.

^* This work was supported by the Agence Nationale de Recherche sur le Syndrome d'Immunodéficience Acquise grant and fellowship (to A.-L. V.). 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 Figs. 1 and 2 and Tables 1–3.

This paper is dedicated to the memory of Dr. Dominique Dormont (Deceased November 16, 2003).

^|| To whom correspondence should be addressed: Laboratoire de Biologie Moléculaire de la Cellule, UMR5161, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, 46, Allée d'Italie, 69364 Lyon Cedex 07, France. Tel.: 33-472728563; Fax: 33-472728674; E-mail: pjalinot{at}ens-lyon.fr.

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