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_name
Virologyjournal_title
Virologyauthors
Bolduan S,Votteler J,Lodermeyer V,Greiner T,Koppensteiner H,Schindler M,Thiel G,Schubert Udoi
10.1016/j.virol.2011.04.009subject
Has Abstractpub_date
2011-07-20 00:00:00pages
75-85issue
1-2eissn
0042-6822issn
1096-0341pii
S0042-6822(11)00189-9journal_volume
416pub_type
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