Antagonism of CD317 Restriction of Human Immunodeficiency Virus Type 1 (HIV-1) Particle Release and Depletion of CD317 Are Separable Activities of HIV-1 Vpu

被引:65
作者
Goffinet, Christine [1 ]
Homann, Stefanie [1 ]
Ambiel, Ina [1 ]
Tibroni, Nadine [1 ]
Rupp, Daniel [1 ]
Keppler, Oliver T. [1 ]
Fackler, Oliver T. [1 ]
机构
[1] Univ Heidelberg, Dept Infect Dis, D-69120 Heidelberg, Germany
关键词
CLATHRIN-MEDIATED ENDOCYTOSIS; DOWN-MODULATION; CELL-SURFACE; TETHERIN; DEGRADATION; MECHANISM; PROTEIN;
D O I
10.1128/JVI.01549-09
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页码:4089 / 4094
页数:6
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