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Ion channel activity of HIV-1 Vpu is dispensable for counteraction of CD317.

Bolduan, Sebastian and Votteler, Jörg and Lodermeyer, Veronika and Greiner, Timo and Koppensteiner, Herwig and Schindler, Michael and Thiel, Gerhard and Schubert, Ulrich (2011):
Ion channel activity of HIV-1 Vpu is dispensable for counteraction of CD317.
In: Virology, 416 (1-2), pp. 75-85, ISSN 1096-0341,
[Article]

Abstract

While the C-terminal domain of HIV-1 Vpu is critical for CD4 degradation, the transmembrane domain (TM) mediates ion channel activity, enhances virus release and is essential for counteracting CD317/Bst-2/Tetherin. Here we analyzed whether the ion channel activity of Vpu is required to antagonize CD317-mediated restriction of virion release. We examined TM-mutants of three conserved residues: the S23A mutation, which was previously shown to abrogate ion channel function, did not affect Vpu mediated augmentation of virus release. In contrast, the A14N and A18N mutation did not affect ion channel activity of Vpu, but substantially reduced its ability to support virus release and to down-regulate CD317 from the cell surface. Altogether, our data suggest that not the ion channel activity of Vpu, but its ability to remove CD317 from the cell surface is required to augment HIV-1 release.

Item Type: Article
Erschienen: 2011
Creators: Bolduan, Sebastian and Votteler, Jörg and Lodermeyer, Veronika and Greiner, Timo and Koppensteiner, Herwig and Schindler, Michael and Thiel, Gerhard and Schubert, Ulrich
Title: Ion channel activity of HIV-1 Vpu is dispensable for counteraction of CD317.
Language: English
Abstract:

While the C-terminal domain of HIV-1 Vpu is critical for CD4 degradation, the transmembrane domain (TM) mediates ion channel activity, enhances virus release and is essential for counteracting CD317/Bst-2/Tetherin. Here we analyzed whether the ion channel activity of Vpu is required to antagonize CD317-mediated restriction of virion release. We examined TM-mutants of three conserved residues: the S23A mutation, which was previously shown to abrogate ion channel function, did not affect Vpu mediated augmentation of virus release. In contrast, the A14N and A18N mutation did not affect ion channel activity of Vpu, but substantially reduced its ability to support virus release and to down-regulate CD317 from the cell surface. Altogether, our data suggest that not the ion channel activity of Vpu, but its ability to remove CD317 from the cell surface is required to augment HIV-1 release.

Journal or Publication Title: Virology
Volume: 416
Number: 1-2
Divisions: 10 Department of Biology > Plant Membrane Biophysics
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10 Department of Biology
Date Deposited: 21 Jun 2011 11:52
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