Evidence map›Paper›PMID 27853288›Full record

ArticleScientific reports2016

Enhancing Virion Tethering by BST2 Sensitizes Productively and Latently HIV-infected T cells to ADCC Mediated by Broadly Neutralizing Antibodies.

Tram N Q Pham, Sabelo Lukhele, Frédéric Dallaire, Gabrielle Perron, Éric A Cohen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Metformin Enhances Antibody-Mediated Recognition of HIV-Infected CD4bioRxiv : the preprint server for biology · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Antibodies for Human Immunodeficiency Virus-1 Cure Strategies.The Journal of infectious diseases · 2021
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Conserved HIV Epitopes for an Effective HIV Vaccine.Journal of clinical & cellular immunology · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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

5 authors at 2 institutions in 1 country.

Tram N Q PhamInstitut de Recherches Cliniques de Montréal, Montréal, Québec, H2W 1R7, Canada.
Sabelo LukheleInstitut de Recherches Cliniques de Montréal, Montréal, Québec, H2W 1R7, Canada.
Frédéric DallaireInstitut de Recherches Cliniques de Montréal, Montréal, Québec, H2W 1R7, Canada.
Gabrielle PerronInstitut de Recherches Cliniques de Montréal, Montréal, Québec, H2W 1R7, Canada.
Éric A CohenInstitut de Recherches Cliniques de Montréal, Montréal, Québec, H2W 1R7, Canada.
Montreal Clinical Research Institute · CAUniversité de Montréal · CA

Funding

CIHR MOP-111226
6 · The paper itself

Abstract

Binding of anti-HIV antibodies (Abs) to envelope (Env) glycoproteins on infected cells can mark them for elimination via antibody-dependent cell-mediated cytotoxicity (ADCC). BST2, a type I interferon (IFN)-stimulated restriction factor that anchors nascent Env-containing virions at the surface of infected cells has been shown to enhance ADCC functions. In a comprehensive analysis of ADCC potency by neutralizing anti-HIV Abs (NAbs), we show in this study that NAbs are capable of mediating ADCC against HIV-infected T cells with 3BNC117, PGT126 and PG9 being most efficient. We demonstrate that HIV-induced BST2 antagonism effectively attenuates Ab binding and ADCC responses mediated by all classes of NAbs that were tested. Interestingly, IFNα treatment can reverse this effect in a BST2-dependent manner. Importantly, while reactivated latent T cell lines display some susceptibility to ADCC mediated by broadly NAbs, inactivating BST2 viral countermeasures and/or exogenous IFNα augment their elimination. Overall, our findings support the notion that NAbs can induce ADCC. They highlight that while BST2 antagonism by HIV promotes ADCC evasion, strategies aimed at restoring BST2 restriction could improve anti-HIV responses and potentially provide a means to eliminate reactivated cells in latent reservoirs.

Indexed as

Antibodies, NeutralizingAntibody-Dependent Cell CytotoxicityAntigens, CDBone Marrow Stromal Antigen 2FemaleGPI-Linked ProteinsHEK293 CellsHIV-1HIV AntibodiesHIV InfectionsHumansMaleT-LymphocytesVirionVirus LatencyAntibodies, NeutralizingAntigens, CDBone Marrow Stromal Antigen 2BST2 protein, humanGPI-Linked ProteinsHIV Antibodies

Identifiers

PMID27853288
PMCPMC5112552
OpenAlexW2556031178

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.