Evidence map›Paper›PMID 31915279›Full record

ArticleJournal of virology2020

PARP1 Enhances Influenza A Virus Propagation by Facilitating Degradation of Host Type I Interferon Receptor.

Chuan Xia, Jennifer J Wolf, Chuankai Sun, Mengqiong Xu, Caleb J Studstill, Jun Chen, Hanh Ngo, Hua Zhu, Bumsuk Hahm

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 46 citations in OpenAlex.

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  7. NADThe Journal of general virology · 2026
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  10. NADFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  11. Article
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  14. Review
  15. Article
  16. The Hemagglutinin of Influenza A Virus Induces Ferroptosis to Facilitate Viral Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  17. Review
  18. Review
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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

9 authors at 2 institutions in 2 countries.

Chuan Xia *Department of Biotechnology, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, China xiachuan@jnu.edu.cn hahmb@health.missouri.edu.
Jennifer J Wolf *Departments of Surgery and Molecular Microbiology and Immunology, University of Missouri, Columbia, Missouri, USA.
Chuankai SunDepartment of Biotechnology, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, China.
Mengqiong XuDepartment of Biotechnology, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, China.
Caleb J StudstillDepartments of Surgery and Molecular Microbiology and Immunology, University of Missouri, Columbia, Missouri, USA.
Jun ChenDepartment of Biotechnology, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, China.
Hanh NgoDepartments of Surgery and Molecular Microbiology and Immunology, University of Missouri, Columbia, Missouri, USA.
Hua ZhuDepartment of Biotechnology, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, China.
Bumsuk HahmDepartments of Surgery and Molecular Microbiology and Immunology, University of Missouri, Columbia, Missouri, USA xiachuan@jnu.edu.cn hahmb@health.missouri.edu.
Jinan University · CNUniversity of Missouri · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Influenza A virus (IAV) utilizes multiple strategies to confront or evade host type I interferon (IFN)-mediated antiviral responses in order to enhance its own propagation within the host. One such strategy is to induce the degradation of type I IFN receptor 1 (IFNAR1) by utilizing viral hemagglutinin (HA). However, the molecular mechanism behind this process is poorly understood. Here, we report that a cellular protein, poly(ADP-ribose) polymerase 1 (PARP1), plays a critical role in mediating IAV HA-induced degradation of IFNAR1. We identified PARP1 as an interacting partner for IAV HA through mass spectrometry analysis. This interaction was confirmed by coimmunoprecipitation analyses. Furthermore, confocal fluorescence microscopy showed altered localization of endogenous PARP1 upon transient IAV HA expression or during IAV infection. Knockdown or inhibition of PARP1 rescued IFNAR1 levels upon IAV infection or HA expression, exemplifying the importance of PARP1 for IAV-induced reduction of IFNAR1. Notably, PARP1 was crucial for the robust replication of IAV, which was associated with regulation of the type I IFN receptor signaling pathway. These results indicate that PARP1 promotes IAV replication by controlling viral HA-induced degradation of host type I IFN receptor. Altogether, these findings provide novel insight into interactions between influenza virus and the host innate immune response and reveal a new function for PARP1 during influenza virus infection.

Indexed as

Influenza A Virus, H1N1 SubtypeA549 CellsAnimalsAntiviral AgentsChlorocebus aethiopsDogsHEK293 CellsHemagglutinin Glycoproteins, Influenza VirusHumansImmunity, InnateInfluenza, HumanMadin Darby Canine Kidney CellsMass SpectrometryMicroscopy, ConfocalPoly (ADP-Ribose) Polymerase-1Receptor, Interferon alpha-betaAntiviral AgentsH1N1 virus hemagglutininHemagglutinin Glycoproteins, Influenza VirusIFNAR1 protein, humanIFNAR2 protein, humanPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Receptor, Interferon alpha-betaRNA, Small Interferinghemagglutinininfluenza A virusPARP1type I interferon receptor

Identifiers

PMID31915279
PMCPMC7081902
OpenAlexW2999010016

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.