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Nef proteins of epidemic HIV-1 group O strains antagonize human tetherin

Most simian immunodeficiency viruses use their Nef protein to antagonize the host restriction factor tetherin. A deletion in human tetherin confers Nef resistance, representing a hurdle to successful zoonotic transmission. HIV-1 group M evolved to utilize the viral protein U (Vpu) to counteract tethe...

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Bibliographic Details
Main Authors: Kluge, Silvia Franziska (Author) , Pujol, Franc̦ois (Author) , Fackler, Oliver Till (Author)
Format: Article (Journal)
Language:English
Published: 12 November 2014
In: Cell host and microbe
Year: 2014, Volume: 16, Issue: 5, Pages: 639-650
ISSN:1934-6069
DOI:10.1016/j.chom.2014.10.002
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.chom.2014.10.002
Verlag, lizenzpflichtig, Volltext: https://linkinghub.elsevier.com/retrieve/pii/S1931312814003801
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Author Notes:Silvia F. Kluge, Katharina Mack, Shilpa S. Iyer, François M. Pujol, Anke Heigele, Gerald H. Learn, Shariq M. Usmani, Daniel Sauter, Simone Joas, Dominik Hotter, Frederic Bibollet-Ruche, Lindsey J. Plenderleith, Martine Peeters, Matthias Geyer, Paul M. Sharp, Oliver T. Fackler, Beatrice H. Hahn, and Frank Kirchhoff
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Summary:Most simian immunodeficiency viruses use their Nef protein to antagonize the host restriction factor tetherin. A deletion in human tetherin confers Nef resistance, representing a hurdle to successful zoonotic transmission. HIV-1 group M evolved to utilize the viral protein U (Vpu) to counteract tetherin. Although HIV-1 group O has spread epidemically in humans, it has not evolved a Vpu-based tetherin antagonism. Here we show that HIV-1 group O Nef targets a region adjacent to this deletion to inhibit transport of human tetherin to the cell surface, enhances virion release, and increases viral resistance to inhibition by interferon-a. The Nef protein of the inferred common ancestor of group O viruses is also active against human tetherin. Thus, Nef-mediated antagonism of human tetherin evolved prior to the spread of HIV-1 group O and likely facilitated secondary virus transmission. Our results may explain the epidemic spread of HIV-1 group O.
Item Description:Gesehen am 11.08.2020
Physical Description:Online Resource
ISSN:1934-6069
DOI:10.1016/j.chom.2014.10.002

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