Evidence map›Paper›PMID 28955326›Full record

ArticleFrontiers in immunology2017

Influenza A Virus PA Antagonizes Interferon-β by Interacting with Interferon Regulatory Factor 3.

Chenyang Yi, Zongzheng Zhao, Shengyu Wang, Xin Sun, Dan Zhang, Xiaomei Sun, Anding Zhang, Meilin Jin

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  5. Review
  6. Review
  7. PA and PA-X: two key proteins from segment 3 of the influenza viruses.Frontiers in cellular and infection microbiology · 2025
    Review
  8. Review
  9. Review
  10. Naturally occurring PAVirologica Sinica · 2024
    Article
  11. Article
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  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

8 authors at 1 institution in 1 country.

Chenyang YiState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Zongzheng ZhaoState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Shengyu WangState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Xin SunState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Dan ZhangState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Xiaomei SunState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Anding ZhangState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Meilin JinState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Huazhong Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The influenza A virus (IAV) can be recognized by retinoic acid-inducible gene I (RIG-I) to activate the type I interferon response and induce antiviral effects. The virus has evolved several strategies to evade the innate immune response, including non-structural protein 1 (NS1) and its polymerase subunits. The mechanism by which NS1 inhibits interferon-β (IFN-β) is well understood, whereas the mechanism by which polymerase acid protein (PA) inhibits IFN-β remains to be elucidated. In this study, we observed that the IAV PA protein could inhibit the production of IFN-β and interferon-stimulated genes induced by Sendai virus through interferon regulatory factor 3 (IRF3), but not through nuclear factor-kappaB (NF-kappaB). In addition, PA inhibited IFN-β induction by RIG-I, melanoma differentiation-associated gene 5, mitochondria antiviral signaling protein, TANK-binding kinase 1, inhibitor of nuclear factor kappa-B kinase-ε (IKKε), and IRF3 overexpression. Furthermore, PA interacted with IRF3 to block its activation. The N-terminal endonuclease activity of PA was responsible for its interaction with IRF3 and inhibition of the IFN-β signaling pathway. In summary, our data reveal the mechanism by which IAV PA inhibits the IFN-β signaling pathway, providing a new mechanism by which the virus antagonizes the antiviral signaling pathway.

Indexed as

innate immunitypdm/09phosphorylationpolymerasesignaling pathway

Identifiers

PMID28955326
PMCPMC5600993
OpenAlexW2755373925

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.