ArticleScientific reports2015
Involvement of a C-terminal motif in the interference of primate lentiviral Vpu proteins with CD1d-mediated antigen presentation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Article
- Review
- Plasma Membrane-Associated Restriction Factors and Their Counteraction by HIV-1 Accessory Proteins.Cells · 2019Review
- 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
- CD1-Restricted T Cells During Persistent Virus Infections: "Sympathy for the Devil".Frontiers in immunology · 2018Review
- Functional conservation and coherence of HIV-1 subtype A Vpu alleles.Scientific reports · 2017Article
- FRET Analysis of the Promiscuous yet Specific Interactions of the HIV-1 Vpu Transmembrane Domain.Biophysical journal · 2017Article
- Various plus unique: Viral protein U as a plurifunctional protein for HIV-1 replication.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- Functional conservation and coherence of HIV-1 subtype A Vpu alleles.Scientific reports · 2017Article
- Innate Invariant NKT Cell Recognition of HIV-1-Infected Dendritic Cells Is an Early Detection Mechanism Targeted by Viral Immune Evasion.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Remodeling of the Host Cell Plasma Membrane by HIV-1 Nef and Vpu: A Strategy to Ensure Viral Fitness and Persistence.Viruses · 2016Review
- Vpu Protein: The Viroporin Encoded by HIV-1.Viruses · 2015Review
- HIV-1 Vpu utilizes both cullin-RING ligase (CRL) dependent and independent mechanisms to downmodulate host proteins.Retrovirology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The HIV-1 accessory protein Vpu is emerging as a critical factor for viral evasion from innate immunity. We have previously shown that the Vpu proteins of two HIV-1 group M subtype B strains (NL4-3 and BaL) down-regulate CD1d from the surface of infected dendritic cells (DCs) and inhibit their crosstalk with the innate invariant natural killer T (iNKT) cells. In the present study, we have investigated the ability of a comprehensive set of primate lentiviral Vpu proteins to interfere with CD1d-mediated immunity. We found that CD1d down-regulation is a conserved function of Vpu proteins from HIV-1 groups M, O and P as well as their direct precursors SIVcpzPtt and SIVgor. At the group M subtype level, subtype C Vpu proteins were significantly weaker CD1d antagonists than subtype B Vpu proteins. Functional characterization of different mutants and chimeras derived from active subtype B and inactive subtype C Vpu proteins revealed that residues in the cytoplasmic domain are important for CD1d down-regulation. Specifically, we identified a C-terminal APW motif characteristic for group M subtype B Vpu proteins necessary for interference with CD1d surface expression. These findings support the notion that Vpu plays an important role in lentiviral evasion from innate immunity.
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Registered trials
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