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Journal of Virology, April 2001, p. 3791-3801, Vol. 75, No. 8
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.8.3791-3801.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Comparison of Cell Cycle Arrest, Transactivation, and Apoptosis Induced by the Simian Immunodeficiency Virus SIVagm and Human Immunodeficiency Virus Type 1 vpr Genes

Yonghong Zhu,1,2 Harris A. Gelbard,3 Mikhail Roshal,1,2 Shannon Pursell,1 Beth D. Jamieson,4 and Vicente Planelles1,2,*

Departments of Medicine,1 Microbiology & Immunology,2 and Neurology,3 University of Rochester Cancer Center, Rochester, New York, and Department of Medicine, University of California, Los Angeles, California4

Received 30 August 2000/Accepted 12 January 2001

All primate lentiviruses known to date contain one or two open reading frames with homology to the human immunodeficiency virus type 1 (HIV-1) vpr gene. HIV-1 vpr encodes a 96-amino-acid protein with multiple functions in the viral life cycle. These functions include modulation of the viral replication kinetics, transactivation of the long terminal repeat, participation in the nuclear import of preintegration complexes, induction of G2 arrest, and induction of apoptosis. The simian immunodeficiency virus (SIV) that infects African green monkeys (SIVagm) contains a vpr homologue, which encodes a 118-amino-acid protein. SIVagm vpr is structurally and functionally related to HIV-1 vpr. The present study focuses on how three specific functions (transactivation, induction of G2 arrest, and induction of apoptosis) are related to one another at a functional level, for HIV-1 and SIVagm vpr. While our study supports previous reports demonstrating a causal relationship between induction of G2 arrest and transactivation for HIV-1 vpr, we demonstrate that the same is not true for SIVagm vpr. Transactivation by SIVagm vpr is independent of cell cycle perturbation. In addition, we show that induction of G2 arrest is necessary for the induction of apoptosis by HIV-1 vpr but that the induction of apoptosis by SIVagm vpr is cell cycle independent. Finally, while SIVagm vpr retains its transactivation function in human cells, it is unable to induce G2 arrest or apoptosis in such cells, suggesting that the cytopathic effects of SIVagm vpr are species specific. Taken together, our results suggest that while the multiple functions of vpr are conserved between HIV-1 and SIVagm, the mechanisms leading to the execution of such functions are divergent.

* Corresponding author. Mailing address: Departments of Medicine and Microbiology & Immunology, University of Rochester Cancer Center, 601 Elmwood Avenue, Box 704, Rochester, NY 14642. Phone: (716) 273-4474. Fax: (716) 273-1221. E-mail: vicente_planelles{at}urmc.rochester.edu.

Journal of Virology, April 2001, p. 3791-3801, Vol. 75, No. 8
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.8.3791-3801.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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