Evidence map›Paper›PMID 19129183›Full record

ArticleThe Journal of biological chemistry2009

The Kaposi's Sarcoma-associated Herpesvirus-encoded vIRF-3 Inhibits Cellular IRF-5.

Effi Wies, Alexander S Hahn, Katharina Schmidt, Cornelia Viebahn, Nadine Rohland, Anja Lux, Tim Schellhorn, Angela Holzer, Jae U Jung, Frank Neipel

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.3field-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

48 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Kaposi sarcoma herpesvirus pathogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  9. Article
  10. Multicentric Castleman disease: Where are we now?Seminars in diagnostic pathology · 2016
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Molecular biology of human herpesvirus 8: novel functions and virus-host interactions implicated in viral pathogenesis and replication.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2014
    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

10 authors at 2 institutions in 2 countries.

Effi WiesVirologisches Institut, Universitätsklinikum Erlangen, D-91054 Erlangen, Germany.
Alexander S Hahn
Katharina Schmidt
Cornelia Viebahn
Nadine Rohland
Anja Lux
Tim Schellhorn
Angela Holzer
Jae U Jung
Frank Neipel
Universitätsklinikum Erlangen · DEUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kaposi's sarcoma-associated herpesvirus encodes four genes with homology to the family of interferon regulatory factors (IRFs). At least one of these viral IRFs, vIRF-3, is expressed in latently Kaposi's sarcoma-associated herpesvirus-infected primary effusion lymphoma (PEL) cells and is essential for the survival of PEL cells. We now report that vIRF-3 interacts with cellular IRF-5, thereby inhibiting binding of IRF-5 to interferon-responsive promoter elements. Consequently, vIRF-3 blocked IRF-5-mediated promoter activation. A central double helix motif present in vIRF-3 was sufficient to abrogate both DNA binding and transcriptional transactivation by IRF-5. Upon DNA damage or activation of the interferon or Toll-like receptor pathways, cytoplasmic IRF-5 has been reported to be translocated to the nucleus, which results in induction of both p53-independent apoptosis and p21-mediated cell cycle arrest. We report here that IRF-5 is present in the nuclei of PEL cells without interferon stimulation. Silencing of vIRF-3 expression in PEL cells was accompanied by increased sensitivity to interferon-mediated apoptosis and up-regulation of IRF-5 target genes. In addition, vIRF-3 antagonized IRF-5-mediated activation of the p21 promoter. The data presented here indicate that vIRF-3 contributes to immune evasion and sustained proliferation of PEL cells by releasing IRF-5 from transcription complexes.

Indexed as

Response ElementsActive Transport, Cell NucleusAmino Acid MotifsApoptosisCell NucleusCyclin-Dependent Kinase Inhibitor p21Gene SilencingHerpesvirus 8, HumanHumansInterferon Regulatory FactorsLymphoma, Primary EffusionProtein BindingReceptors, InterferonSarcoma, KaposiToll-Like ReceptorsTranscriptional ActivationCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Interferon Regulatory FactorsIRF5 protein, humanReceptors, InterferonToll-Like ReceptorsTP53 protein, humanTumor Suppressor Protein p53viral interferon regulatory factorsViral Proteins

Identifiers

PMID19129183
PMCPMC2659211
OpenAlexW2035906476

What OpenQuestion holds

Textmetadata
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.