Evidence map›Paper›PMID 31076606›Full record

ArticleScientific reports2019

PA-X antagonises MAVS-dependent accumulation of early type I interferon messenger RNAs during influenza A virus infection.

Rachel E Rigby, Helen M Wise, Nikki Smith, Paul Digard, Jan Rehwinkel

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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
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  4. PA and PA-X: two key proteins from segment 3 of the influenza viruses.Frontiers in cellular and infection microbiology · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
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  11. Review
  12. Article
  13. Review
  14. Accessory Gene Products of Influenza A Virus.Cold Spring Harbor perspectives in medicine · 2021
    Review
  15. Article
  16. Article
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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

5 authors at 2 institutions in 1 country.

Rachel E RigbyMedical Research Council Human Immunology Unit, Medical Research Council Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK.ORCID http://orcid.org/0000-0001-5201-9422
Helen M WiseThe Roslin Institute & Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, UK.
Nikki SmithThe Roslin Institute & Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, UK.
Paul DigardThe Roslin Institute & Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, UK.
Jan RehwinkelMedical Research Council Human Immunology Unit, Medical Research Council Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK. jan.rehwinkel@imm.ox.ac.uk.
Roslin Institute · GBUniversity of Oxford · GB

Funding

Biotechnology and Biological Sciences Research Council BB/J004324/1Biotechnology and Biological Sciences Research Council BB/P013740/1Medical Research Council MC_UU_00008/8Medical Research Council MC_UU_12010/8
6 · The paper itself

Abstract

The sensing of viral nucleic acids by the innate immune system activates a potent antiviral response in the infected cell, a key component of which is the expression of genes encoding type I interferons (IFNs). Many viruses counteract this response by blocking the activation of host nucleic acid sensors. The evolutionarily conserved influenza A virus (IAV) protein PA-X has been implicated in suppressing the host response to infection, including the expression of type I IFNs. Here, we characterise this further using a PA-X-deficient virus of the mouse-adapted PR8 strain to study activation of the innate immune response in a mouse model of the early response to viral infection. We show that levels of Ifna4 and Ifnb1 mRNAs in the lungs of infected mice were elevated in the absence of PA-X and that this was completely dependent on MAVS. This therefore suggests a role for PA-X in preventing the accumulation of early type I IFN mRNAs in the lung during IAV infection.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsImmunity, InnateInfluenza A virusInterferon Type ILungMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutOrthomyxoviridae InfectionsRepressor ProteinsRNA, MessengerSignal TransductionToll-Like Receptor 7Viral Nonstructural ProteinsAdaptor Proteins, Signal TransducingInterferon Type IMAVS protein, mouseMembrane GlycoproteinsPA-X protein, influenza A virusRepressor ProteinsRNA, MessengerTlr7 protein, mouseToll-Like Receptor 7Viral Nonstructural Proteins

Identifiers

PMID31076606
PMCPMC6510759
OpenAlexW2944745586

What OpenQuestion holds

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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.