Evidence map›Paper›PMID 26172439›Full record

ArticlePLoS pathogens2015

Vpu Exploits the Cross-Talk between BST2 and the ILT7 Receptor to Suppress Anti-HIV-1 Responses by Plasmacytoid Dendritic Cells.

Mariana G Bego, Édouard Côté, Nick Aschman, Johanne Mercier, Winfried Weissenhorn, Éric A Cohen

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Type I Interferon Production of Plasmacytoid Dendritic Cells under Control.International journal of molecular sciences · 2021
    Review
  9. Review
  10. Infection and cancer suppress pDC derived IFN-I.Current opinion in immunology · 2020
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Limiting Respiratory Viral Infection by Targeting Antiviral and Immunological Functions of BST-2/Tetherin: Knowledge and Gaps.BioEssays : news and reviews in molecular, cellular and developmental biology · 2018
    Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Mariana G BegoInstitut de Recherches Cliniques de Montréal (IRCM), Montreal, Quebec, Canada.
Édouard CôtéInstitut de Recherches Cliniques de Montréal (IRCM), Montreal, Quebec, Canada.
Nick AschmanUniversité Grenoble Alpes, Unit of Virus Host Cell Interactions (UVHCI), CNRS, UVHCI, Grenoble, France.
Johanne MercierInstitut de Recherches Cliniques de Montréal (IRCM), Montreal, Quebec, Canada.
Winfried WeissenhornUniversité Grenoble Alpes, Unit of Virus Host Cell Interactions (UVHCI), CNRS, UVHCI, Grenoble, France.
Éric A CohenInstitut de Recherches Cliniques de Montréal (IRCM), Montreal, Quebec, Canada; Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.
Montreal Clinical Research Institute · CAUnit of Virus Host Cell Interactions · FRUniversité Grenoble Alpes · FR

Funding

CIHR 111226-1CIHR 133050-1CIHR MOP-111226
6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDCs) constitute a major source of type-I interferon (IFN-I) production during acute HIV infection. Their activation results primarily from TLR7-mediated sensing of HIV-infected cells. However, the interactions between HIV-infected T cells and pDCs that modulate this sensing process remain poorly understood. BST2/Tetherin is a restriction factor that inhibits HIV release by cross-linking virions onto infected cell surface. BST2 was also shown to engage the ILT7 pDC-specific inhibitory receptor and repress TLR7/9-mediated IFN-I production by activated pDCs. Here, we show that Vpu, the HIV-1 antagonist of BST2, suppresses TLR7-mediated IFN-I production by pDC through a mechanism that relies on the interaction of BST2 on HIV-producing cells with ILT7. Even though Vpu downregulates surface BST2 as a mean to counteract the restriction on HIV-1 release, we also find that the viral protein re-locates remaining BST2 molecules outside viral assembly sites where they are free to bind and activate ILT7 upon cell-to-cell contact. This study shows that through a targeted regulation of surface BST2, Vpu promotes HIV-1 release and limits pDC antiviral responses upon sensing of infected cells. This mechanism of innate immune evasion is likely to be important for an efficient early viral dissemination during acute infection.

Indexed as

Antigens, CDBone Marrow Stromal Antigen 2CD4-Positive T-LymphocytesCell LineCoculture TechniquesDendritic CellsFlow CytometryGPI-Linked ProteinsHIV-1HIV InfectionsHuman Immunodeficiency Virus ProteinsHumansImmune EvasionMicroscopy, ConfocalReceptor Cross-TalkReceptors, ImmunologicAntigens, CDBone Marrow Stromal Antigen 2BST2 protein, humanGPI-Linked ProteinsHuman Immunodeficiency Virus ProteinsLILRA4 protein, humanReceptors, ImmunologicViral Regulatory and Accessory ProteinsViroporin Proteinsvpu protein, Human immunodeficiency virus 1

Identifiers

PMID26172439
PMCPMC4501562
OpenAlexW1802930479

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.