ArticleProceedings of the National Academy of Sciences of the United States of America2009
Vpu enhances HIV-1 virus release in the absence of Bst-2 cell surface down-modulation and intracellular depletion.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers.
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Who cites it
170 citing papers in PubMed.
- Preservation of tetherin and CD4 counter-activities in circulating Vpu alleles despite extensive sequence variation within HIV-1 infected individuals.PLoS pathogens · 2014Trial
- HIV-1 Vpu interacts with RBM10 to promote HIV-1 infection.mSystems · 2025Article
- CD317 functions as a key antiviral factor in human herpesvirus 6 (HHV-6) infection.Journal of virology · 2025Article
- Involvement of Human Cellular Proteins and Structures in Realization of the HIV Life Cycle: A Comprehensive Review, 2024.Viruses · 2024Review
- Mechanisms of Innate Immune Sensing of HTLV-1 and Viral Immune Evasion.Pathogens (Basel, Switzerland) · 2023Review
- HIV-Host Cell Interactions.Cells · 2023Review
- FastMix: a versatile data integration pipeline for cell type-specific biomarker inference.Bioinformatics (Oxford, England) · 2022Article
- Detection of the HIV-1 Accessory Proteins Nef and Vpu by Flow Cytometry Represents a New Tool to Study Their Functional Interplay within a Single Infected CD4Journal of virology · 2022Article
- Simian Immunodeficiency Virus SIVgsn-99CM71 Vpu Employs Different Amino Acids To Antagonize Human and Greater Spot-Nosed Monkey BST-2.Journal of virology · 2022Article
- Viral Aggregation: The Knowns and Unknowns.Viruses · 2022Review
- HIV replication and latency in monocytes and macrophages.Seminars in immunology · 2021Review
- Epigenetic Regulation ofFrontiers in immunology · 2021Article
- The viral protein U (Vpu)-interacting host protein ATP6V0C down-regulates cell-surface expression of tetherin and thereby contributes to HIV-1 release.The Journal of biological chemistry · 2020Article
- Vpu of a Simian Immunodeficiency Virus Isolated from Greater Spot-Nosed Monkey Antagonizes Human BST-2 via Two AxxxxxxxW Motifs.Journal of virology · 2020Article
- HIV-1 Impairment via UBE3A and HIV-1 Nef Interactions Utilizing the Ubiquitin Proteasome System.Viruses · 2019Article
- Severe acute respiratory syndrome coronavirus spike protein counteracts BST2-mediated restriction of virus-like particle release.Journal of medical virology · 2019Article
- Role of the Ubiquitin Proteasome System (UPS) in the HIV-1 Life Cycle.International journal of molecular sciences · 2019Review
- Contribution of the Cytoplasmic Determinants of Vpu to the Expansion of Virus-Containing Compartments in HIV-1-Infected Macrophages.Journal of virology · 2019Article
- The C-Terminal End of HIV-1 Vpu Has a Clade-Specific Determinant That Antagonizes BST-2 and Facilitates Virion Release.Journal of virology · 2019Article
- Mechanism of Tetherin Inhibition of Alphavirus Release.Journal of virology · 2019Article
110 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
HIV-1 Vpu enhances the release of virions from infected cells. Recent work identified Bst-2/CD317/tetherin as a host factor whose inhibitory activity on viral release is counteracted by Vpu. A current working model proposes that Bst-2 inhibits virus release by tethering viral particles to the cell surface. Here, we analyzed endogenous Bst-2 with respect to its effect on virus release from HeLa cells, T cells, and macrophages. We noted significant cell type-dependent variation in Bst-2 expression. Vpu caused a reduction in Bst-2 expression in transfected HeLa cells and long-term infected macrophages. However, Vpu expression did not result in cell surface down-modulation of Bst-2 or a reduction in intracellular Bst-2 expression in CEMx174 or H9 cells, yet virus replication in these cells was Vpu-responsive. Surprisingly, Bst-2 was undetectable in cell-free virions that were recovered from the surface of HeLa cells by physical shearing, suggesting that a tethering model may not explain all of the functional properties of Bst-2. Taken together we conclude that enhancement of virus release by Vpu does not, at least in CEMx174 and H9 cells, require cell surface down-modulation or intracellular depletion of Bst-2, nor does it entail exclusion of Bst-2 from viral particles.
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