ArticleThe Journal of infectious diseases2017
Emergence of Novel Human Norovirus GII.17 Strains Correlates With Changes in Blockade Antibody Epitopes.
Article in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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.
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Who cites it
27 citing papers in PubMed, 51 citations in OpenAlex.
- Emergence of a novel GII.17 variant is associated with immune evasion rather than an altered HBGA-binding profile.PLoS pathogens · 2026Article
- GII.17 norovirus re-emerged in the 2020s as a result of dynamic and adaptive evolutionary processes.Nature communications · 2025Article
- Delayed Emergence of Norovirus GII.17 in Finland: Foodborne Outbreaks Reported During the 2024/25 Season.Viruses · 2025Article
- Molecular Evolution and Epidemiology of Norovirus GII.4 Viruses in the United States.The Journal of infectious diseases · 2025Article
- Appearance and spread of norovirus genotype GII.17 subcluster C2 (Romania-2021 like) in Nizhny Novgorod, Russia, 2021-2023.Archives of virology · 2025Article
- The saga to monitor and control norovirus: the rise of GII.17.The Journal of general virology · 2025Review
- Detection of human noroviruses in sewage by next generation sequencing in Shandong Province, 2019-2021.Virology journal · 2025Article
- Noroviruses: Evolutionary Dynamics, Epidemiology, Pathogenesis, and Vaccine Advances-A Comprehensive Review.Vaccines · 2024Review
- Identification of a GII.6 norovirus blockade antibody epitope.Virus research · 2023Article
- Infant antibody and B-cell responses following confirmed pediatric GII.17 norovirus infections functionally distinguish GII.17 genetic clusters.Frontiers in immunology · 2023Article
- Article
- Rapid screening for antigenic characterization of GII.17 norovirus strains with variations in capsid gene.Gut pathogens · 2022Article
- Identification of a blockade epitope of human norovirus GII.17.Emerging microbes & infections · 2021Article
- Genome-wide analyses of human noroviruses provide insights on evolutionary dynamics and evidence of coexisting viral populations evolving under recombination constraints.PLoS pathogens · 2021Article
- Evolutionary Mechanism of Immunological Cross-Reactivity Between Different GII.17 Variants.Frontiers in microbiology · 2021Article
- Article
- Molecular evolution of GII.P17-GII.17 norovirus associated with sporadic acute gastroenteritis cases during 2013-2018 in Zhoushan Islands, China.Virus genes · 2020Article
- Human Norovirus Proteins: Implications in the Replicative Cycle, Pathogenesis, and the Host Immune Response.Frontiers in immunology · 2020Review
- Molecular and evolutionary characterization of norovirus GII.17 in the northern region of Brazil.BMC infectious diseases · 2019Article
- Norovirus Activity and Genotypes in Sporadic Acute Diarrhea in Children in Shanghai During 2014-2018.The Pediatric infectious disease journal · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Background: Human norovirus is a significant public health burden, with >30 genotypes causing endemic levels of disease and strains from the GII.4 genotype causing serial pandemics as the virus evolves new ligand binding and antigenicity features. During 2014-2015, genotype GII.17 cluster IIIb strains emerged as the leading cause of norovirus infection in select global locations. Comparison of capsid sequences indicates that GII.17 is evolving at previously defined GII.4 antibody epitopes. Methods: Antigenicity of virus-like particles (VLPs) representative of clusters I, II, and IIIb GII.17 strains were compared by a surrogate neutralization assay based on antibody blockade of ligand binding. Results: Sera from mice immunized with a single GII.17 VLP identified antigenic shifts between each cluster of GII.17 strains. Ligand binding of GII.17 cluster IIIb VLP was blocked only by antisera from mice immunized with cluster IIIb VLPs. Exchange of residues 393-396 from GII.17.2015 into GII.17.1978 ablated ligand binding and altered antigenicity, defining an important varying epitope in GII.17. Conclusions: The capsid sequence changes in GII.17 strains result in loss of blockade antibody binding, indicating that viral evolution, specifically at residues 393-396, may have contributed to the emergence of cluster IIIb strains and the persistence of GII.17 in human populations.
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