Evidence map›Paper›PMID 29281104›Full record

ArticleThe Journal of infectious diseases2018

Antigenic Characterization of a Novel Recombinant GII.P16-GII.4 Sydney Norovirus Strain With Minor Sequence Variation Leading to Antibody Escape.

Lisa C Lindesmith, Paul D Brewer-Jensen, Michael L Mallory, Kari Debbink, Excel W Swann, Jan Vinjé, Ralph S Baric

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 36 citations in OpenAlex.

  1. Phylogenetic Analyses ofMicroorganisms · 2026
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  17. Virus-Host Interactions Between Nonsecretors and Human Norovirus.Cellular and molecular gastroenterology and hepatology · 2020
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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

7 authors at 3 institutions in 1 country.

Lisa C LindesmithDepartment of Epidemiology, University of North Carolina, Chapel Hill.
Paul D Brewer-JensenDepartment of Epidemiology, University of North Carolina, Chapel Hill.
Michael L MalloryDepartment of Epidemiology, University of North Carolina, Chapel Hill.
Kari DebbinkDepartment of Natural Sciences, Bowie State University, Maryland.
Excel W SwannDepartment of Epidemiology, University of North Carolina, Chapel Hill.
Jan VinjéDivision of Viral Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia.
Ralph S BaricDepartment of Epidemiology, University of North Carolina, Chapel Hill.
University of North Carolina at Chapel Hill · USBowie State University · USCenters for Disease Control and Prevention · US

Funding

Virology, Immunology, and Microbiology CoreP30AI050410 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAVID M. MARGOLIS · 2001 to 2026
$76.9M
Translational CoreU19AI109761 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BARIC, RALPH S · 2014 to 2018
$32.6M
Mechanisms of Norovirus Protective ImmunityR56AI106006 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BARIC, RALPH S · 2014 to 2014
$760k
NIAID NIH HHS P30 AI050410NIAID NIH HHS R56 AI106006NIAID NIH HHS U19 AI109761Wellcome TrustWellcome Trust A17-0915-001
6 · The paper itself

Abstract

Background: Human noroviruses are the leading cause of acute gastroenteritis. Strains of the GII.4 genotype cause pandemic waves associated with viral evolution and subsequent antigenic drift and ligand-binding modulation. In November 2015, a novel GII.4 Sydney recombinant variant (GII.P16-GII.4 Sydney) emerged and replaced GII.Pe-GII.4 Sydney as the predominant cause of acute gastroenteritis in the 2016-2017 season in the United States. Methods: Virus-like particles of GII.4 2012 and GII.4 2015 were compared for ligand binding and antibody reactivity, using a surrogate neutralization assay. Results: Residue changes in the capsid between GII.4 2012 and GII.4 2015 decreased the potency of human polyclonal sera and monoclonal antibodies. A change in epitope A resulted in the complete loss of reactivity of a class of blockade antibodies and reduced levels of a second antibody class. Epitope D changes modulated monoclonal antibody potency and ligand-binding patterns. Conclusions: Substitutions in blockade antibody epitopes between GII.4 2012 and GII.4 2015 influenced antigenicity and ligand-binding properties. Although the impact of polymerases on fitness remains uncertain, antigenic variation resulting in decreased potency of antibodies to epitope A, coupled with altered ligand binding, likely contributed significantly to the spread of GII.4 2015 and its replacement of GII.4 2012 as the predominant norovirus outbreak strain.

Indexed as

Antigenic VariationAmino Acid SequenceAntibodies, ViralAntibody AffinityAntigens, ViralModels, MolecularNorovirusProtein BindingProtein ConformationAntibodies, ViralAntigens, Viral

Identifiers

PMID29281104
PMCPMC5939617
OpenAlexW2777819235

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.