ArticleFrontiers in microbiology2022
Epidemiological Impact of GII.17 Human Noroviruses Associated With Attachment to Enterocytes.
Article in Frontiers in microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 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
- Multi-Ligand Interactions Shape Human Norovirus Persistence, Transmission, and Control in Food Matrices.Viruses · 2026Review
- Emergence and predominance of GII.17[P17] noroviruses in Brazil, 2023-2024.Scientific reports · 2026Article
- Recovery of infectious recombinant human norovirus using zebrafish embryos.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- GII.17 norovirus re-emerged in the 2020s as a result of dynamic and adaptive evolutionary processes.Nature communications · 2025Article
- The saga to monitor and control norovirus: the rise of GII.17.The Journal of general virology · 2025Review
- Norovirus replication, host interactions and vaccine advances.Nature reviews. Microbiology · 2025Review
- Review
- Intestinal Norovirus Binding Patterns in Nonsecretor Individuals.Journal of virology · 2022Article
- Antiviral strategies against human norovirus: Molecular targets, therapeutics, and vaccine development.Therapeutic advances in infectious diseaseReview
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For the last 30 years, molecular surveys have shown that human norovirus (HuNoV), predominantly the GII.4 genotype, is one of the main causative agents of gastroenteritis. However, epidemiological surveys have revealed the worldwide emergence of GII.17 HuNoVs. Genetic analysis confirmed that GII.17 strains are distributed into three variants (i.e., Kawasaki 308, Kawasaki 323, and CS-E1). Here, virus-like particles (VLPs) were baculovirus-expressed from these variants to study putative interactions with HBGA. Qualitative analysis of the HBGA binding profile of each variant showed that the most recent and predominant GII.17 variant, Kawasaki 308, possesses a larger binding spectrum. The retrospective study of GII.17 strains documented before the emergence of the dominant Kawasaki 308 variant showed that the emergence of a new GII.17 variant could be related to an increased binding capacity toward HBGA. The use of duodenal histological sections confirmed that recognition of enterocytes involved HBGA for the three GII.17 variants. Finally, we observed that the relative affinity of recent GII.17 VLPs for HBGA remains lower than that of the GII.4-2012 variant. These observations suggest a model whereby a combination of virological factors, such as polymerase fidelity and increased affinity for HBGA, and immunological factors was responsible for the incomplete and non-persistent replacement of GII.4 by new GII.17 variants.
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