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Originally published In Press as doi:10.1074/jbc.M205313200 on July 2, 2002

J. Biol. Chem., Vol. 277, Issue 40, 37820-37831, October 4, 2002
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HIV-1 Vpr Induces Apoptosis through Caspase 9 in T Cells and Peripheral Blood Mononuclear Cells*

Karuppiah Muthumani, Daniel S. Hwang, Brijal M. Desai, Donghui Zhang, Nathanael Dayes, Douglas R. GreenDagger , and David B. Weiner§

From the Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, the Dagger  La Jolla Institute for Allergy and Immunology, San Diego, California 92121, and  Viral Genomix, Philadelphia, Pennsylvania 19104

Human immunodeficiency virus, type 1 (HIV-1), vpr gene encodes a 14-kDa virion-associated protein, which exhibits significant effects on human cells. One important property of Vpr is its ability to induce apoptosis during infection. Apoptotic induction is likely to play a role in the pathogenesis of AIDS. However, the pathway of apoptosis is not clearly defined. In this report we investigate the mechanism of apoptosis induced by HIV-1 Vpr using a Vpr pseudotype viral infection system or adeno delivery of Vpr in primary human lymphoid cells and T-cells. With either vector, HIV-1 Vpr induced cell cycle arrest at the G2/M phase and apoptosis in lymphoid target cells. Furthermore, we observed that with both vectors, caspase 9, but not caspase 8, was activated following infection of human peripheral blood mononuclear cell with either Vpr-positive HIV virions or adeno-delivered Vpr. Activation of the caspase 9 pathway resulted in caspase 3 activation and apoptosis in human primary cells. These effects were coincident with the disruption of the mitochondrial transmembrane potential and induction of cytochrome c release by Vpr. The Vpr-induced signaling pathway did not induce CD95 or CD95L expression. Bcl-2 overexpressing cells succumb to Vpr-induced apoptosis. These studies illustrate that Vpr induces a mitochondria-dependent apoptotic pathway that is distinct from apoptosis driven by the Fas-FasL pathway.

* This work was supported by grants from the National Institutes of Health (to D. B. W.) and the University of Pennsylvania Center for Aids Research Core Laboratories.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.

§ To whom correspondence should be addressed: Dept. of Pathology and Laboratory Medicine, University of Pennsylvania, 505 Stellar Chance Laboratories, 422 Curie Blvd., Philadelphia, PA 19104. Tel.: 215-662-2352; Fax: 215-573-9436; E-mail: dbweiner@mail.med.upenn.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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