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Originally published In Press as doi:10.1074/jbc.M002198200 on November 28, 2000

J. Biol. Chem., Vol. 276, Issue 9, 6359-6369, March 2, 2001
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Attachment of Human Immunodeficiency Virus-1 (HIV-1) Particles Bearing Host-encoded B7-2 Proteins Leads to Nuclear Factor-kappa B- and Nuclear Factor of Activated T Cells-dependent Activation of HIV-1 Long Terminal Repeat Transcription*

Salim BounouDagger , Nancy Dumais, and Michel J. Tremblay§

From the Centre de Recherche en Infectiologie, Centre Hospitalier Universitaire de Québec, Pavillon CHUL, and Département de Biologie médicale, Faculté de Médecine, Université Laval, Ste-Foy, Québec G1V 4G2, Canada

Previous studies have shown that human immunodeficiency virus type-1 (HIV-1) can incorporate several surface proteins of host origin. Recent findings indicate that host-encoded cell surface constituents retain their functionality when found embedded into the viral envelope. The primary objective of the current study was to define whether interaction between some specific virion-bound host proteins with their natural cognate ligands present on target cells could mediate intracellular signaling cascade(s). For this purpose, we have generated a whole series of isogenic virus stocks (NL4-3 backbone) bearing or not bearing on their surface foreign CD28, CD54 (ICAM-1), CD80 (B7-1) or CD86 (B7-2) proteins. Our results indicate that incubation of human T lymphoid cells with virions bearing host-derived B7-2 proteins and anti-CD3 antibody can potently activate HIV-1 long terminal repeat-driven gene expression. This up-regulating effect necessitates the involvement of nuclear factor-kappa B (NF-kappa B) and nuclear factor of activated T cells (NFAT) as revealed by the use of vectors coding for dominant negative versions of both transcription factors (i.e. Ikappa Balpha S32A/36A and dnNFAT) and band shift assays. The increase of NF-kappa B activity was abolished when infection with B7-2-bearing HIV-1 particles was performed in the presence of the fusion protein CTLA-4 Ig suggesting that the interaction between virally embedded B7-2 and CD28 on the target cell is responsible for the observed NF-kappa B induction. The findings presented here provide the first demonstration that host-encoded proteins acquired by HIV-1 can mediate signal transduction events.

* This work was supported in part by Canadian Institutes of Health Research HIV/AIDS Research Program Grant HOP-14438 and by a Fonds de la Recherche en Santé du Québec (Réseau FRSQ SIDA et Maladies Infectieuses) grant (both to M. J. T.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Recipient of a Ph.D. fellowship from the Fonds de la Recherche en Santé du Québec/Fonds pour la Formation de chercheurs et l'Aide à la Recherche-Program Santé. This work was performed in partial fulfillment of the requirements for a Ph.D. degree at the Faculty of Graduate Studies, Department of Medical Biology, Faculty of Medicine, Laval University.

§ Holder of a Canada Research Chair in Human Immuno Retrovirology. To whom correspondence should be addressed: Laboratoire d'ImmunoRétrovirologie Humaine, Centre de Recherche en Infectiologie, RC709, Centre Hospitalier Universitaire de Québec, Pavillon CHUL, 2705 boul. Laurier, Ste-Foy, Québec G1V 4G2, Canada. Tel.: 418-654-2705; Fax: 418-654-2212; E-mail: michel.j.tremblay@crchul.ulaval.ca.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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