Evidence map›Paper›PMID 23761407›Full record

ArticleThe Journal of general virology2013

Vaccinia virus protein N2 is a nuclear IRF3 inhibitor that promotes virulence.

Brian J Ferguson, Camilla T O Benfield, Hongwei Ren, Vivian H Lee, Gordon L Frazer, Pavla Strnadova, Rebecca P Sumner, Geoffrey L Smith

Open access · greenAbstract read
In one paragraph

Article in The Journal of general virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

55 citing papers in PubMed, 85 citations in OpenAlex.

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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 2 institutions in 1 country.

Brian J FergusonDepartment of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK.
Camilla T O BenfieldDepartment of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK.
Hongwei RenDepartment of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK.
Vivian H LeeDepartment of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK.
Gordon L FrazerDepartment of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, UK.
Pavla StrnadovaDepartment of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK.
Rebecca P SumnerDepartment of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK.
Geoffrey L SmithDepartment of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK.
University of Cambridge · GBImperial College London · GB

Funding

Medical Research CouncilWellcome Trust 090315
6 · The paper itself

Abstract

Vaccinia virus (VACV) expresses many proteins that are non-essential for virus replication but promote virulence by inhibiting components of the host immune response to infection. These immunomodulators include a family of proteins that have, or are predicted to have, a structure related to the B-cell lymphoma (Bcl)-2 protein. Five members of the VACV Bcl-2 family (N1, B14, A52, F1 and K7) have had their crystal structure solved, others have been characterized and a function assigned (C6, A46), and others are predicted to be Bcl-2 proteins but are uncharacterized hitherto (N2, B22, C1). Data presented here show that N2 is a nuclear protein that is expressed early during infection and inhibits the activation of interferon regulatory factor (IRF)3. Consistent with its nuclear localization, N2 inhibits IRF3 downstream of the TANK-binding kinase (TBK)-1 and after IRF3 translocation into the nucleus. A mutant VACV strain Western Reserve lacking the N2L gene (vΔN2) showed normal replication and spread in cultured cells compared to wild-type parental (vN2) and revertant (vN2-rev) viruses, but was attenuated in two murine models of infection. After intranasal infection, the vΔN2 mutant induced lower weight loss and signs of illness, and virus was cleared more rapidly from the infected tissue. In the intradermal model of infection, vΔN2 induced smaller lesions that were resolved more rapidly. In summary, the N2 protein is an intracellular virulence factor that inhibits IRF3 activity in the nucleus.

Indexed as

Host-Pathogen InteractionsAnimalsDisease Models, AnimalFemaleGene DeletionInterferon Regulatory Factor-3MiceMice, Inbred BALB CVacciniaVaccinia virusViral ProteinsVirulenceVirulence FactorsVirus ReplicationInterferon Regulatory Factor-3Irf3 protein, mouseViral ProteinsVirulence Factors

Identifiers

PMID23761407
PMCPMC3749055
OpenAlexW2048955142

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.