Evidence map›Paper›PMID 25211330›Full record

ArticlePLoS pathogens2014

The Tudor domain protein Spindlin1 is involved in intrinsic antiviral defense against incoming hepatitis B Virus and herpes simplex virus type 1.

Aurélie Ducroux, Shirine Benhenda, Lise Rivière, O John Semmes, Monsef Benkirane, Christine Neuveut

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Structural basis of the hepatitis B virus X protein in complex with DDB1.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Review
  5. The role of HBV cccDNA in occult hepatitis B virus infection.Molecular and cellular biochemistry · 2023
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Driving integrative structural modeling with serial capture affinity purification.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Aurélie DucrouxUnité des Hépacivirus et Immunité Innée, Institut Pasteur, Paris, France; UMR CNRS 3569, Paris, France.
Shirine BenhendaUnité des Hépacivirus et Immunité Innée, Institut Pasteur, Paris, France; UMR CNRS 3569, Paris, France.
Lise RivièreUnité des Hépacivirus et Immunité Innée, Institut Pasteur, Paris, France; UMR CNRS 3569, Paris, France.
O John SemmesThe Leroy T. Canoles Jr Cancer Research Center and Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia, United States of America.
Monsef BenkiraneInstitut de Génétique Humaine, CNRS UPR 1142, Laboratoire de Virologie Moléculaire, Montpellier, France.
Christine NeuveutUnité des Hépacivirus et Immunité Innée, Institut Pasteur, Paris, France; UMR CNRS 3569, Paris, France.
Centre National de la Recherche Scientifique · FRInstitut Pasteur · FRCancer Research Center · US

Funding

HTLV-I TAX MEDIATED DEREGULATION OF CELL STATER01CA076595 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI SEMMES, OLIVER JOHN · 1999 to 2016
$2.9M
NCI NIH HHS R01 CA076595
6 · The paper itself

Abstract

Hepatitis B virus infection (HBV) is a major risk factor for the development of hepatocellular carcinoma. HBV replicates from a covalently closed circular DNA (cccDNA) that remains as an episome within the nucleus of infected cells and serves as a template for the transcription of HBV RNAs. The regulatory protein HBx has been shown to be essential for cccDNA transcription in the context of infection. Here we identified Spindlin1, a cellular Tudor-domain protein, as an HBx interacting partner. We further demonstrated that Spindlin1 is recruited to the cccDNA and inhibits its transcription in the context of infection. Spindlin1 knockdown induced an increase in HBV transcription and in histone H4K4 trimethylation at the cccDNA, suggesting that Spindlin1 impacts on epigenetic regulation. Spindlin1-induced transcriptional inhibition was greater for the HBV virus deficient for the expression of HBx than for the HBV WT virus, suggesting that HBx counteracts Spindlin1 repression. Importantly, we showed that the repressive role of Spindlin1 is not limited to HBV transcription but also extends to other DNA virus that replicate within the nucleus such as Herpes Simplex Virus type 1 (HSV-1). Taken together our results identify Spindlin1 as a critical component of the intrinsic antiviral defense and shed new light on the function of HBx in HBV infection.

Indexed as

Antiviral AgentsBlotting, NorthernBlotting, WesternCarcinoma, HepatocellularCell Cycle ProteinsCells, CulturedDNA, ViralHepatitis BHepatitis B virusHerpes SimplexHerpesvirus 1, HumanHumansImmunoprecipitationLiver NeoplasmsMicrotubule-Associated ProteinsPhosphoproteinsAntiviral AgentsCell Cycle ProteinsDNA, ViralMicrotubule-Associated ProteinsPhosphoproteinsRNA, Messengerspindlin

Identifiers

PMID25211330
PMCPMC4161474
OpenAlexW2035572185

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.