Evidence map›Paper›PMID 17301153›Full record

ArticleJournal of virology2007

Rotavirus NSP1 inhibits expression of type I interferon by antagonizing the function of interferon regulatory factors IRF3, IRF5, and IRF7.

Mario Barro, John T Patton

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 2% 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

123 citing papers in PubMed, 1 synthesis or guideline pooled it, 203 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Microorganisms · 2023
    Article
  12. Article
  13. Article
  14. iScience · 2023
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

63 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Mario BarroLaboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, 50 South Drive, Bethesda, MD 20892-8026, USA.
John T Patton
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Modification Of The Antigenicity & Virulence Of Rotaviruses By Reverse GeneticsZIAAI000788 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI PATTON, JOHN · 2009 to 2015
$4.2M
MODIFICATION OF THE ANTIGENICITY &VIRULENCE OF ROTAVIRUSES BY REVERSE GENETICSZ01AI000788 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI PATTON, JOHN · 1997 to 2008
$1.1M
Intramural NIH HHS
6 · The paper itself

Abstract

Secretion of interferon (IFN) by virus-infected cells is essential for activating autocrine and paracrine pathways that promote cellular transition to an antiviral state. In most mammalian cells, IFN production is initiated by the activation of constitutively expressed IFN regulatory factor 3, IRF3, which in turn leads to the induction of IRF7, the "master regulator" of IFN type I synthesis (alpha/beta IFN). Previous studies established that rotavirus NSP1 antagonizes IFN signaling by inducing IRF3 degradation. In the present study, we have determined that, in comparison to wild-type rotaviruses, rotaviruses encoding defective NSP1 grow to lower titers in some cell lines and that this poor growth phenotype is due to their failure to suppress IFN expression. Furthermore, we provide evidence that rotaviruses encoding wild-type NSP1 subvert IFN signaling by inducing the degradation of not only IRF3, but also IRF7, with both events occurring through proteasome-dependent processes that proceed with similar efficiencies. The capacity of NSP1 to induce IRF7 degradation may allow rotavirus to move across the gut barrier by enabling the virus to replicate in specialized trafficking cells (dendritic cells and macrophages) that constitutively express IRF7. Along with IRF3 and IRF7, NSP1 was found to induce the degradation of IRF5, a factor that upregulates IFN expression and that is involved in triggering apoptosis during viral infection. Our analysis suggests that NSP1 mediates the degradation of IRF3, IRF5, and IRF7 by recognizing a common element of IRF proteins, thereby allowing NSP1 to act as a broad-spectrum antagonist of IRF function.

Indexed as

Amino Acid SequenceAnimalsBlotting, WesternCaco-2 CellsGene ComponentsGene Expression RegulationHumansInterferon Regulatory FactorsInterferon Type IMacaca mulattaMicroscopy, FluorescenceMolecular Sequence DataRotavirus InfectionsSequence AlignmentSignal TransductionViral Nonstructural ProteinsInterferon Regulatory FactorsInterferon Type Insp1 protein, RotavirusViral Nonstructural Proteins

Identifiers

PMID17301153
PMCPMC1900170
OpenAlexW2102683798

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.