Journal
JOURNAL OF VIROLOGY
Volume 84, Issue 8, Pages 4089-4094Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01549-09
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Funding
- Peter and Traudl Engelhorn-Stiftung
- Medical Faculty of Heidelberg
- Graduate Academy of Heidelberg University
- CellNetworks Cluster of Excellence [EXC81]
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Vpu antagonizes human immunodeficiency virus type 1 (HIV-1) particle release inhibition by CD317/BST2/Tetherin. Whether this Vpu activity strictly requires cellular depletion of the restriction factor is unclear. Here, we characterized CD317 variants with mutations in putative sorting or ubiquitination motifs. All mutants still potently impaired release of Vpu-defective HIV-1 and remained sensitive to Vpu-mediated release enhancement. Importantly, this virological antagonism correlated with surface downregulation of CD317 mutants by Vpu, while intracellular pools of these mutants, which were consistently depleted of the wild-type protein, were highly variable or even enhanced. Thus, Vpu can efficiently antagonize virion tethering in the absence of CD317 degradation.
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