Evidence map›Paper›PMID 35533151›Full record

ArticlePLoS pathogens2022

TRIM25 and ZAP target the Ebola virus ribonucleoprotein complex to mediate interferon-induced restriction.

Rui Pedro Galão, Harry Wilson, Kristina L Schierhorn, Franka Debeljak, Bianca S Bodmer, Daniel Goldhill, Thomas Hoenen, Sam J Wilson, Chad M Swanson, Stuart J D Neil

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 47 citations in OpenAlex.

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  20. A minimal complex of KHNYN and zinc-finger antiviral protein binds and degrades single-stranded RNA.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

10 authors at 4 institutions in 2 countries.

Rui Pedro GalãoDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, United Kingdom.ORCID 0000-0003-3368-5053
Harry WilsonDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, United Kingdom.ORCID 0000-0002-3185-1073
Kristina L SchierhornDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, United Kingdom.ORCID 0000-0002-8649-1394
Franka DebeljakDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, United Kingdom.
Bianca S BodmerInstitute for Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Greifswald, Germany.ORCID 0000-0001-9695-9168
Daniel GoldhillSection of Virology, Department of Medicine, Imperial College London, London, United Kingdom.ORCID 0000-0003-4597-5963
Thomas HoenenInstitute for Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Greifswald, Germany.ORCID 0000-0002-5829-6305
Sam J WilsonMRC Centre for Virus Research, University of Glasgow, United Kingdom.ORCID 0000-0002-6065-0895
Chad M SwansonDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, United Kingdom.ORCID 0000-0002-6650-3634
Stuart J D NeilDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, United Kingdom.ORCID 0000-0003-3306-5831
King's College London · GBFriedrich-Loeffler-Institut · DEImperial College London · GBMRC University of Glasgow Centre for Virus Research · GB

Funding

Medical Research Council MC/PC/15068Medical Research Council MC_PC_15068Medical Research Council MC_UU_12014/10Medical Research Council MR/M019756/1Medical Research Council MR/S000844/1Wellcome TrustWellcome Trust WT098049AIA
6 · The paper itself

Abstract

Ebola virus (EBOV) causes highly pathogenic disease in primates. Through screening a library of human interferon-stimulated genes (ISGs), we identified TRIM25 as a potent inhibitor of EBOV transcription-and-replication-competent virus-like particle (trVLP) propagation. TRIM25 overexpression inhibited the accumulation of viral genomic and messenger RNAs independently of the RNA sensor RIG-I or secondary proinflammatory gene expression. Deletion of TRIM25 strongly attenuated the sensitivity of trVLPs to inhibition by type-I interferon. The antiviral activity of TRIM25 required ZAP and the effect of type-I interferon was modulated by the CpG dinucleotide content of the viral genome. We find that TRIM25 interacts with the EBOV vRNP, resulting in its autoubiquitination and ubiquitination of the viral nucleoprotein (NP). TRIM25 is recruited to incoming vRNPs shortly after cell entry and leads to dissociation of NP from the vRNA. We propose that TRIM25 targets the EBOV vRNP, exposing CpG-rich viral RNA species to restriction by ZAP.

Indexed as

EbolavirusHemorrhagic Fever, EbolaInterferon Type IAnimalsAntiviral AgentsRibonucleoproteinsTripartite Motif ProteinsUbiquitin-Protein LigasesVirus ReplicationAntiviral AgentsInterferon Type IRibonucleoproteinsTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID35533151
PMCPMC9119685
OpenAlexW4229441458

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.