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Journal of Virology, January 1999, p. 778-782, Vol. 73, No. 1
0022-538X/99/$00.00+0

Lack of Effect of Cytoplasmic Tail Truncations on Human Immunodeficiency Virus Type 2 ROD Env Particle Release Activity

Stephan P. Bour,* Claudia Aberham, Christèle Perrin, and Klaus Strebel

Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892-0460

Received 15 June 1998/Accepted 30 September 1998

In addition to its role in receptor binding, the envelope glycoprotein of certain human immunodeficiency virus type 2 (HIV-2) isolates, including ROD10, exhibits a biological activity that enhances the release of HIV-2, HIV-1, and simian immunodeficiency virus particles from infected cells. The present study aims at better defining the functional domains involved in this biological activity. To this end, we have characterized the envelope protein of the ROD14 isolate of HIV-2, which, despite 95% homology with the ROD10 envelope at the amino acid level, is unable to enhance viral particle release. Site-directed mutagenesis showed that the presence of a truncation in the cytoplasmic tail of the ROD14 envelope was not responsible for the lack of activity, as previously reported for the HIV-2 ST isolate (G. D. Ritter, Jr., G. Yamshchikov, S. J. Cohen, and M. J. Mulligan, J. Virol. 70:2669-2673, 1996). Similarly, several modifications of the length of the ROD10 envelope cytoplasmic tail did not impair its ability to enhance particle release, suggesting that, in the case of the HIV-2 ROD isolate, particle release activity is not regulated by the length of the cytoplasmic tail.

* Corresponding author. Mailing address: NIH/NIAID, Building 4, Room 312, 9000 Rockville Pike, Bethesda, MD 20892-0460. Phone: (301) 496-3132. Fax: (301) 402-0226. E-mail: sbour{at}nih.gov.

Journal of Virology, January 1999, p. 778-782, Vol. 73, No. 1
0022-538X/99/$00.00+0


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