Evidence map›Paper›PMID 31511615›Full record

ArticleScientific reports2019

HIV-1 Vpr mediates the depletion of the cellular repressor CTIP2 to counteract viral gene silencing.

F Forouzanfar, S Ali, C Wallet, M De Rovere, C Ducloy, H El Mekdad, M El Maassarani, A Aït-Ammar, J Van Assche, E Boutant and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Microglial Cells: The Main HIV-1 Reservoir in the Brain.Frontiers in cellular and infection microbiology · 2019
    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

16 authors at 6 institutions in 3 countries.

F ForouzanfarUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France.
S AliUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France.
C WalletUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France.
M De RovereUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France.
C DucloyINSERM U1109, Fédération de Médecine Translationnelle (FMTS), Université de Strasbourg, Strasbourg, France.
H El MekdadUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France.
M El MaassaraniUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France.
A Aït-AmmarUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France.
J Van AsscheUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France.
E BoutantUniversité de Strasbourg, UMR 7021 CNRS, Illkirch, France.
F DaouadUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France.
F Margottin-GoguetInserm, U1016, Institut Cochin, 22 rue Méchain, 75014, Paris, France.ORCID http://orcid.org/0000-0002-3124-6690
C MoogINSERM U1109, Fédération de Médecine Translationnelle (FMTS), Université de Strasbourg, Strasbourg, France.
C Van LintUniversité Libre de Bruxelles (ULB), Service of Molecular Virology, Department of Molecular Biology (DBM), Gosselies, Belgium. cvlint@ulb-ac.be.
C SchwartzUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France. christian.schwartz@unistra.fr.
O RohrUniversité de Strasbourg, EA7292, FMTS, IUT Louis Pasteur, Schiltigheim, France. olivier.rohr@unistra.fr.ORCID http://orcid.org/0000-0001-8992-2025
Université de Strasbourg · FRInserm · FRUniversité Libre de Bruxelles · BECentre National de la Recherche Scientifique · FRDélégation Paris 5 · FRUniversity of Agriculture Faisalabad · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammals have evolved many antiviral factors impacting different steps of the viral life cycle. Associated with chromatin-modifying enzymes, the cellular cofactor CTIP2 contributes to HIV-1 gene silencing in latently infected reservoirs that constitute the major block toward an HIV cure. We report, for the first time, that the virus has developed a strategy to overcome this major transcriptional block. Productive HIV-1 infection results in a Vpr-mediated depletion of CTIP2 in microglial cells and CD4+ T cells, two of the major viral reservoirs. Associated to the Cul4A-DDB1-DCAF1 ubiquitin ligase complex, Vpr promotes CTIP2 degradation via the proteasome pathway in the nuclei of target cells and notably at the latent HIV-1 promoter. Importantly, Vpr targets CTIP2 associated with heterochromatin-promoting enzymes dedicated to HIV-1 gene silencing. Thereby, Vpr reactivates HIV-1 expression in a microglial model of HIV-1 latency. Altogether our results suggest that HIV-1 Vpr mediates the depletion of the cellular repressor CTIP2 to counteract viral gene silencing.

Indexed as

Gene SilencingCell LineCells, CulturedGene Expression Regulation, ViralHEK293 CellsHIV-1HIV InfectionsHost-Pathogen InteractionsHumansJurkat CellsProteasome Endopeptidase ComplexProtein BindingProteolysisRepressor ProteinsTumor Suppressor ProteinsVirus LatencyBCL11B protein, humanProteasome Endopeptidase ComplexRepressor ProteinsTumor Suppressor Proteinsvpr Gene Products, Human Immunodeficiency Virus

Identifiers

PMID31511615
PMCPMC6739472
OpenAlexW2973087665

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.