Evidence map›Paper›PMID 26566030›Full record

ArticlePLoS pathogens2015

PML/TRIM19-Dependent Inhibition of Retroviral Reverse-Transcription by Daxx.

Jacques Dutrieux, Ghizlane Maarifi, Débora M Portilho, Nathalie J Arhel, Mounira K Chelbi-Alix, Sébastien Nisole

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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Capsid-host interactions for HIV-1 ingress.Microbiology and molecular biology reviews : MMBR · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. STAT1 and Its Crucial Role in the Control of Viral Infections.International journal of molecular sciences · 2022
    Review
  14. SUMOylation in Viral Replication and Antiviral Defense.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Review
  15. Review
  16. Review
  17. Review
  18. Viruses in the Nucleus.Cold Spring Harbor perspectives in biology · 2021
    Review
  19. Review
  20. The Roles of TRIMs in Antiviral Innate Immune Signaling.Frontiers in cellular and infection microbiology · 2021
    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 2 institutions in 1 country.

Jacques DutrieuxParis Descartes University, Paris, France.
Ghizlane MaarifiParis Descartes University, Paris, France.
Débora M PortilhoUniversity Institute of Hematology, Saint-Louis Hospital, Paris, France.
Nathalie J ArhelUniversity Institute of Hematology, Saint-Louis Hospital, Paris, France.
Mounira K Chelbi-AlixParis Descartes University, Paris, France.
Sébastien NisoleParis Descartes University, Paris, France.
Université Paris Cité · FRDélégation Paris 5 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PML (Promyelocytic Leukemia protein), also known as TRIM19, belongs to the family of tripartite motif (TRIM) proteins. PML is mainly expressed in the nucleus, where it forms dynamic structures known as PML nuclear bodies that recruit many other proteins, such as Sp100 and Daxx. While the role of PML/TRIM19 in antiviral defense is well documented, its effect on HIV-1 infection remains unclear. Here we show that infection by HIV-1 and other retroviruses triggers the formation of PML cytoplasmic bodies, as early as 30 minutes post-infection. Quantification of the number and size of PML cytoplasmic bodies revealed that they last approximately 8 h, with a peak at 2 h post-infection. PML re-localization is blocked by reverse-transcription inhibitors and is not observed following infection with unrelated viruses, suggesting it is specifically triggered by retroviral reverse-transcription. Furthermore, we show that PML interferes with an early step of retroviral infection since PML knockdown dramatically increases reverse-transcription efficiency. We demonstrate that PML does not inhibit directly retroviral infection but acts through the stabilization of one of its well-characterized partners, Daxx. In the presence of PML, cytoplasmic Daxx is found in the vicinity of incoming HIV-1 capsids and inhibits reverse-transcription. Interestingly, Daxx not only interferes with exogenous retroviral infections but can also inhibit retrotransposition of endogenous retroviruses, thus identifying Daxx as a broad cellular inhibitor of reverse-transcription. Altogether, these findings unravel a novel antiviral function for PML and PML nuclear body-associated protein Daxx.

Indexed as

Adaptor Proteins, Signal TransducingCell NucleusCo-Repressor ProteinsHIV-1HumansMolecular ChaperonesNuclear ProteinsPromyelocytic Leukemia ProteinProtein BindingTranscription FactorsTranscription, GeneticTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingCo-Repressor ProteinsDAXX protein, humanMolecular ChaperonesNuclear ProteinsPML protein, humanPromyelocytic Leukemia ProteinTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID26566030
PMCPMC4643962
OpenAlexW2176631207

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.