Evidence map›Paper›PMID 24971589›Full record

ArticlePloS one2014

Host competence and helicase activity differences exhibited by West Nile viral variants expressing NS3-249 amino acid polymorphisms.

Stanley A Langevin, Richard A Bowen, William K Reisen, Christy C Andrade, Wanichaya N Ramey, Payal D Maharaj, Michael Anishchenko, Joan L Kenney, Nisha K Duggal, Hannah Romo and 6 more

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

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  16. Comparative Vector Competence of North AmericanThe American journal of tropical medicine and hygiene · 2018
    Article
  17. Article
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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

16 authors.

Stanley A LangevinCenter for Vectorborne Diseases and Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, California, United States of America.
Richard A BowenDepartment of Biomedical Sciences, Colorado State University, Fort Collins, Colorado, United States of America.
William K ReisenCenter for Vectorborne Diseases and Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, California, United States of America.
Christy C AndradeCenter for Vectorborne Diseases and Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, California, United States of America.
Wanichaya N RameyCenter for Vectorborne Diseases and Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, California, United States of America.
Payal D MaharajCenter for Vectorborne Diseases and Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, California, United States of America.
Michael AnishchenkoDivision of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado, United States of America.
Joan L KenneyDivision of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado, United States of America.
Nisha K DuggalDivision of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado, United States of America.
Hannah RomoDivision of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado, United States of America.
Aloke Kumar BeraDepartment of Biological Sciences, Purdue University, West Lafayette, Indiana, United States of America.
Todd A SandersUnited States Fish and Wildlife Service, Portland, Oregon, United States of America.
Angela Bosco-LauthDepartment of Biomedical Sciences, Colorado State University, Fort Collins, Colorado, United States of America; Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado, United States of America.
Janet L SmithDepartment of Biological Chemistry, University of Michigan, Ann Arbor, Michigan, United States of America.
Richard KuhnDepartment of Biological Sciences, Purdue University, West Lafayette, Indiana, United States of America.
Aaron C BraultCenter for Vectorborne Diseases and Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, California, United States of America; Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado, United States of America.

Funding

Persistence of West Nile virus in CaliforniaR01AI055607 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI REISEN, WILLIAM K · 2003 to 2012
$4.4M
West Nile Viral Determinants of Avian PathogenesisR01AI061822 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI BRAULT, AARON COLE · 2004 to 2007
$1.3M
West Nile Virus Genotypic Affect on Host CompetenceR01CI000235 · CI · UNIVERSITY OF CALIFORNIA DAVIS · PI BRAULT, AARON COLE · 2004 to 2006
$181k
NCPDCID CDC HHS R01 CI000235NCPDCID CDC HHS UO1 CI000235NIAID NIH HHS AI061822NIAID NIH HHS R01 AI055607NIAID NIH HHS R01 AI061822NIAID NIH HHS R01-AI55607
6 · The paper itself

Abstract

A single helicase amino acid substitution, NS3-T249P, has been shown to increase viremia magnitude/mortality in American crows (AMCRs) following West Nile virus (WNV) infection. Lineage/intra-lineage geographic variants exhibit consistent amino acid polymorphisms at this locus; however, the majority of WNV isolates associated with recent outbreaks reported worldwide have a proline at the NS3-249 residue. In order to evaluate the impact of NS3-249 variants on avian and mammalian virulence, multiple amino acid substitutions were engineered into a WNV infectious cDNA (NY99; NS3-249P) and the resulting viruses inoculated into AMCRs, house sparrows (HOSPs) and mice. Differential viremia profiles were observed between mutant viruses in the two bird species; however, the NS3-249P virus produced the highest mean peak viral loads in both avian models. In contrast, this avian modulating virulence determinant had no effect on LD50 or the neurovirulence phenotype in the murine model. Recombinant helicase proteins demonstrated variable helicase and ATPase activities; however, differences did not correlate with avian or murine viremia phenotypes. These in vitro and in vivo data indicate that avian-specific phenotypes are modulated by critical viral-host protein interactions involving the NS3-249 residue that directly influence transmission efficiency and therefore the magnitude of WNV epizootics in nature.

Indexed as

Amino Acid SubstitutionHost SpecificityAmino Acid SequenceAnimalsChlorocebus aethiopsCrowsDEAD-box RNA HelicasesMiceMolecular Sequence DataNucleoside-TriphosphatasePolymorphism, Single NucleotideRNA HelicasesSerine EndopeptidasesSparrowsVero CellsViral Nonstructural ProteinsDEAD-box RNA HelicasesNS3 protein, flavivirusNucleoside-TriphosphataseRNA HelicasesSerine EndopeptidasesViral Nonstructural ProteinsViral Proteases

Identifiers

PMID24971589
PMCPMC4074097

What OpenQuestion holds

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Registered trials

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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.