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Journal of Virology, December 1999, p. 9992-9999, Vol. 73, No. 12
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

A Conserved Dileucine-Containing Motif in p6gag Governs the Particle Association of Vpx and Vpr of Simian Immunodeficiency Viruses SIVmac and SIVagm

Molly A. Accola,1 Anatoly A. Bukovsky,1 Morris S. Jones,1 and Heinrich G. Göttlinger1,2,*

Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute,1 and Department of Pathology, Harvard Medical School,2 Boston, Massachusetts 02115

Received 15 March 1999/Accepted 29 August 1999

Vpr is a small accessory protein of human and simian immunodeficiency viruses (HIV and SIV) that is specifically incorporated into virions. Members of the HIV-2/SIVsm/SIVmac lineage of primate lentiviruses also incorporate a related protein designated Vpx. We previously identified a highly conserved L-X-X-L-F sequence near the C terminus of the p6 domain of the Gag precursor as the major virion association motif for HIV-1 Vpr. In the present study, we show that a different leucine-containing motif (D-X-A-X-X-L-L) in the N-terminal half of p6gag is required for the incorporation of SIVmac Vpx. Similarly, the uptake of SIVmac Vpr depended primarily on the D-X-A-X-X-L-L motif. SIVmac Vpr was unstable when expressed alone, but its intracellular steady-state levels increased significantly in the presence of wild-type Gag or of the proteasome inhibitor lactacystin. Collectively, our results indicate that the interaction with the Gag precursor via the D-X-A-X-X-L-L motif diverts SIVmac Vpr away from the proteasome-degradative pathway. While absent from HIV-1 p6gag, the D-X-A-X-X-L-L motif is conserved in both the HIV-2/SIVsm/SIVmac and SIVagm lineages of primate lentiviruses. We found that the incorporation of SIVagm Vpr, like that of SIVmac Vpx, is absolutely dependent on the D-X-A-X-X-L-L motif, while the L-X-X-L-F motif used by HIV-1 Vpr is dispensable. The similar requirements for the incorporation of SIVmac Vpx and SIVagm Vpr provide support for their proposed common ancestry.

* Corresponding author. Mailing address: Dana-Farber Cancer Institute, 44 Binney St., Boston, MA 02115. Phone: (617) 632-3067. Fax: (617) 632-3113. E-mail: Heinrich_Gottlinger{at}DFCI.harvard.edu.

Journal of Virology, December 1999, p. 9992-9999, Vol. 73, No. 12
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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