The envelope glycoprotein of human immunodeficiency virus type 2 enhances viral particle release: a Vpu-like factor?

1996 ◽  
Vol 70 (2) ◽  
pp. 820-829 ◽  
Author(s):  
S Bour ◽  
U Schubert ◽  
K Peden ◽  
K Strebel
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Envelope Glycoprotein ◽  
Viral Particle ◽  
Particle Release ◽  
Immunodeficiency Virus

Human immunodeficiency virus type 2 envelope glycoprotein: Differential CD4 interactions of soluble gpl20 versus the assembled envelope complex

Virology ◽  
1992 ◽  
Vol 187 (1) ◽  
pp. 233-241 ◽  
Author(s):  
Mark J. Mulligan ◽  
G.Douglas Ritter ◽  
Margery A. Chaikinj ◽  
Galina V. Yamshchikov ◽  
Prasanna Kumar ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Envelope Glycoprotein ◽  
Immunodeficiency Virus

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

1999 ◽  
Vol 73 (1) ◽  
pp. 778-782 ◽  
Author(s):  
Stephan P. Bour ◽  
Claudia Aberham ◽  
Christèle Perrin ◽  
Klaus Strebel
Keyword(s):  
Human Immunodeficiency Virus ◽  
Biological Activity ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Amino Acid Level ◽  
Cytoplasmic Tail ◽  
Site Directed Mutagenesis ◽  
Particle Release ◽  
Immunodeficiency Virus

ABSTRACT 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.

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