Evidence map›Paper›PMID 23269788›Full record

ArticleJournal of virology2013

Both genome segments contribute to the pathogenicity of very virulent infectious bursal disease virus.

Olivier Escaffre, Cyril Le Nouën, Michel Amelot, Xavier Ambroggio, Kristen M Ogden, Olivier Guionie, Didier Toquin, Hermann Müller, Mohammed R Islam, Nicolas Eterradossi

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.5field-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

48 citing papers in PubMed, 115 citations in OpenAlex.

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  16. The Formation and Function ofInternational journal of molecular sciences · 2023
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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 5 institutions in 4 countries.

Olivier EscaffreAnses-French Agency for Food, Environmental and Occupational Health and Safety, Avian and Rabbit Virology, Immunology and Parasitology Unit (VIPAC), OIE Reference Laboratory for Infectious Bursal Disease, Ploufragan, France.
Cyril Le Nouën
Michel Amelot
Xavier Ambroggio
Kristen M Ogden
Olivier Guionie
Didier Toquin
Hermann Müller
Mohammed R Islam
Nicolas Eterradossi
Agence Nationale de Sécurité Sanitaire de l’Alimentation, de l’Environnement et du Travail · FRBangladesh Agricultural University · BDLeipzig University · DENational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infectious bursal disease virus (IBDV) causes an economically significant disease of chickens worldwide. Very virulent IBDV (vvIBDV) strains have emerged and induce as much as 60% mortality. The molecular basis for vvIBDV pathogenicity is not understood, and the relative contributions of the two genome segments, A and B, to this phenomenon are not known. Isolate 94432 has been shown previously to be genetically related to vvIBDVs but exhibits atypical antigenicity and does not cause mortality. Here the full-length genome of 94432 was determined, and a reverse genetics system was established. The molecular clone was rescued and exhibited the same antigenicity and reduced pathogenicity as isolate 94432. Genetically modified viruses derived from 94432, whose vvIBDV consensus nucleotide sequence was restored in segment A and/or B, were produced, and their pathogenicity was assessed in specific-pathogen-free chickens. We found that a valine (position 321) that modifies the most exposed part of the capsid protein VP2 critically modified the antigenicity and partially reduced the pathogenicity of 94432. However, a threonine (position 276) located in the finger domain of the virus polymerase (VP1) contributed even more significantly to attenuation. This threonine is partially exposed in a hydrophobic groove on the VP1 surface, suggesting possible interactions between VP1 and another, as yet unidentified molecule at this amino acid position. The restored vvIBDV-like pathogenicity was associated with increased replication and lesions in the thymus and spleen. These results demonstrate that both genome segments influence vvIBDV pathogenicity and may provide new targets for the attenuation of vvIBDVs.

Indexed as

Amino Acid SequenceAnimalsBase SequenceBirnaviridae InfectionsChick EmbryoChickensInfectious bursal disease virusMolecular Dynamics SimulationPoultry DiseasesSequence Analysis, RNASpleenThymus GlandViral Structural ProteinsViral Structural ProteinsVP1 protein, infectious bursal disease virusVP2 protein, infectious bursal disease virus

Identifiers

PMID23269788
PMCPMC3571395
OpenAlexW2009695225

What OpenQuestion holds

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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.