Evidence map›Paper›PMID 40219968›Full record

ArticleNucleic acids research2025

Nuclear AGO2 supports influenza A virus replication through type-I interferon regulation.

Hsiang-Chi Huang, Michelle Fong, Iwona Nowak, Evgeniia Shcherbinina, Vivian Lobo, Danica F Besavilla, Hang T Huynh, Karin Schön, Jakub O Westholm, Carola Fernandez and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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

16 authors.

Hsiang-Chi HuangDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Michelle FongDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Iwona NowakDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Evgeniia ShcherbininaDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Vivian LoboDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Danica F BesavillaDepartment of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Hang T HuynhDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Karin SchönDepartment of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Jakub O WestholmDepartment of Biochemistry and Biophysics, National Bioinformatics Infrastructure Sweden, Science for Life Laboratory, Stockholm University, Box 1031, SE-17121 Solna, Sweden.
Carola FernandezDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Angana A H PatelWallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Clotilde WielDepartment of Surgery, Institute of Clinical Sciences, Sahlgrenska Center for Cancer Research, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Volkan I SayinWallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.
Dimitrios G AnastasakisDepartment of Basic Sciences, School of Medicine, University of Crete, GR 70013 Heraklion ,Greece.
Davide AngelettiDepartment of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.ORCID 0000-0002-5256-1972
Aishe A SarshadDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, SE-40530 Gothenburg, Sweden.ORCID 0000-0001-7153-5959

Funding

European Research Council 850638Knut and Alice Wallenberg FoundationKnut and Alice Wallenberg Foundation 2021.0033Knut och Alice Wallenbergs StiftelseSwedish Research Council 2021-01164Swedish Society for Medical Research S19-0019
6 · The paper itself

Abstract

The role of Argonaute (AGO) proteins and the RNA interference (RNAi) machinery in mammalian antiviral response has been debated. Therefore, we set out to investigate how mammalian RNAi impacts influenza A virus (IAV) infection. We reveal that IAV infection triggers nuclear accumulation of AGO2, which is directly facilitated by p53 activation. Mechanistically, we show that IAV induces nuclear AGO2 targeting of TRIM71and type-I interferon-pathway genes for silencing. Accordingly, Tp53-/- mice do not accumulate nuclear AGO2 and demonstrate decreased susceptibility to IAV infection. Hence, the RNAi machinery is highjacked by the virus to evade the immune system and support viral replication. Furthermore, the FDA-approved drug, arsenic trioxide, prevents p53 nuclear translocation, increases interferon response and decreases viral replication in vitro and in a mouse model in vivo. Our data indicate that targeting the AGO2:p53-mediated silencing of innate immunity may offer a promising strategy to mitigate viral infections.

Indexed as

Argonaute ProteinsInfluenza A virusInterferon Type IVirus ReplicationAnimalsCell NucleusHumansImmunity, InnateInfluenza, HumanMiceMice, KnockoutOrthomyxoviridae InfectionsRNA InterferenceTumor Suppressor Protein p53AGO2 protein, humanAgo2 protein, mouseArgonaute ProteinsInterferon Type ITumor Suppressor Protein p53

Identifiers

PMID40219968
PMCPMC11992678

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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.