Evidence map›Paper›PMID 21937657›Full record

ArticleJournal of virology2011

Nonconsensus West Nile virus genomes arising during mosquito infection suppress pathogenesis and modulate virus fitness in vivo.

Gregory D Ebel, Kelly A Fitzpatrick, Pei-Yin Lim, Corey J Bennett, Eleanor R Deardorff, Greta V S Jerzak, Laura D Kramer, Yangsheng Zhou, Pei-Yong Shi, Kristen A Bernard

Abstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 27 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

10 authors at 3 institutions in 1 country.

Gregory D EbelDepartment of Pathology, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA. gebel@salud.unm.edu
Kelly A Fitzpatrick
Pei-Yin Lim
Corey J Bennett
Eleanor R Deardorff
Greta V S Jerzak
Laura D Kramer
Yangsheng Zhou
Pei-Yong Shi
Kristen A Bernard
New York State Department of Health · USUniversity of New Mexico · USWadsworth Center · US

Funding

Viral Pathogenesis and TherapeuticsU54AI057158 · NIAID · WADSWORTH CENTER · PI LIPKIN, W. IAN · 2003 to 2014
$100.8M
FAIR Data Competency and Machine Learning Readiness for Biomedical ScientistsK12GM088021 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI REBECCA S. HARTLEY, Diane Lidke · 2009 to 2026
$16.4M
Quasispecies dynamics in arbovirus persistence emergence and fitnessR01AI067380 · NIAID · UNIVERSITY OF NEW MEXICO · PI Gregory David Ebel · 2007 to 2026
$7.7M
US BASED COLLABORATION IN EMERGING VIRAL AND PRION DISEASES-266025490N01AI025490 · NIAID · HEALTH RESEARCH, INC. · 2003 to 2004
–
NIAID NIH HHS AI067380NIAID NIH HHS N01 AI025490NIAID NIH HHS N01-AI25490NIAID NIH HHS R01 AI067380NIAID NIH HHS U54 AI057158NIAID NIH HHS U54-AI057158NIGMS NIH HHS K12 GM088021NIGMS NIH HHS K12GM088021
6 · The paper itself

Abstract

West Nile virus (WNV) is similar to other RNA viruses in that it forms genetically complex populations within hosts. The virus is maintained in nature in mosquitoes and birds, with each host type exerting distinct influences on virus populations. We previously observed that prolonged replication in mosquitoes led to increases in WNV genetic diversity and diminished pathogenesis in mice without remarkable changes to the consensus genome sequence. We therefore sought to evaluate the relationships between individual and group phenotypes in WNV and to discover novel viral determinants of pathogenesis in mice and fitness in mosquitoes and birds. Individual plaque size variants were isolated from a genetically complex population, and mutations conferring a small-plaque and mouse-attenuated phenotype were localized to the RNA helicase domain of the NS3 protein by reverse genetics. The mutation, an Asp deletion, did not alter type I interferon production in the host but rendered mutant viruses more susceptible to interferon compared to wild type (WT) WNV. Finally, we used an in vivo fitness assay in Culex quinquefasciatus mosquitoes and chickens to determine whether the mutation in NS3 influenced fitness. The fitness of the NS3 mutant was dramatically lower in chickens and moderately lower in mosquitoes, indicating that RNA helicase is a major fitness determinant of WNV and that the effect on fitness is host specific. Overall, this work highlights the complex relationships that exist between individual and group phenotypes in RNA viruses and identifies RNA helicase as an attenuation and fitness determinant in WNV.

Indexed as

Genome, ViralAnimalsCells, CulturedChickensChlorocebus aethiopsCricetinaeCulicidaeDEAD-box RNA HelicasesFemaleFibroblastsGenetic VariationInterferonsKidneyMiceMice, Inbred C3HMutationDEAD-box RNA HelicasesInterferonsNS3 protein, flavivirusNucleoside-TriphosphataseRNA HelicasesRNA, ViralSerine EndopeptidasesViral Nonstructural ProteinsViral Proteases

Identifiers

PMID21937657
PMCPMC3209405
OpenAlexW2120284954

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.