ArticleScientific reports2017
Adaptive mutations of neuraminidase stalk truncation and deglycosylation confer enhanced pathogenicity of influenza A viruses.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- A Novel Recombinant Chicken-Derived H6N8 Subtype Avian Influenza Virus Caused Disease in Chickens and Mice.Viruses · 2025Article
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- Deglycosylation and truncation in the neuraminidase stalk are functionally equivalent in enhancing the pathogenicity of a high pathogenicity avian influenza virus in chickens.Journal of virology · 2025Article
- Article
- Multiple transatlantic incursions of highly pathogenic avian influenza clade 2.3.4.4b A(H5N5) virus into North America and spillover to mammals.Cell reports · 2024Article
- Receptor Binding Properties of Neuraminidase for influenza A virus: An Overview of Recent Research Advances.Virulence · 2023Review
- Phylogenetic analysis and docking study of neuraminidase gene of influenza A/H1N1 viruses circulating in Iran from 2010 to 2019.Virus research · 2023Article
- Assessing compatibility and viral fitness between poultry-adapted H9N2 and wild bird-derived neuraminidases.Scientific reports · 2023Article
- Revisiting influenza A virus life cycle from a perspective of genome balance.Virologica Sinica · 2023Review
- Broadly Protective Neuraminidase-Based Influenza Vaccines and Monoclonal Antibodies: Target Epitopes and Mechanisms of Action.Viruses · 2023Review
- Development of the H3N2 influenza microneedle vaccine for cross-protection against antigenic variants.Scientific reports · 2022Article
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- Article
- Influenza Neuraminidase Characteristics and Potential as a Vaccine Target.Frontiers in immunology · 2021Review
- Review
- H9N2 Influenza Virus Infections in Human Cells Require a Balance between Neuraminidase Sialidase Activity and Hemagglutinin Receptor Affinity.Journal of virology · 2020Article
- Passage of influenza A/H3N2 viruses in human airway cells removes artefactual variants associated with neuraminidase-mediated binding.The Journal of general virology · 2020Article
- Animal models for the risk assessment of viral pandemic potential.Laboratory animal research · 2020Review
- Truncation or Deglycosylation of the Neuraminidase Stalk Enhances the Pathogenicity of the H5N1 Subtype Avian Influenza Virus in Mallard Ducks.Frontiers in microbiology · 2020Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been noticed that neuraminidase (NA) stalk truncation has arisen from evolutionary adaptation of avian influenza A viruses (IAVs) from wild aquatic birds to domestic poultry. We identified this molecular alteration after the adaptation of a 2009 pandemic H1N1 virus (pH1N1) in BALB/c mice. The mouse-adapted pH1N1 lost its eight consecutive amino acids including one potential N-linked glycosite from the NA stalk region. To explore the relationship of NA stalk truncation or deglycosylation with viral pathogenicity changes, we generated NA stalk mutant viruses on the pH1N1 backbone by reverse genetics. Intriguingly, either NA stalk truncation or deglycosylation changed pH1N1 into a lethal virus to mice by resulting in extensive pathologic transformation in the mouse lungs and systemic infection affecting beyond the respiratory organs in mice. The increased pathogenicity of these NA stalk mutants was also reproduced in ferrets. In further investigation using a human-infecting H7N9 avian IAV strain, NA stalk truncation or deglycosylation enhanced the replication property and pathogenicity of H7N9 NA stalk mutant viruses in the same mouse model. Taken together, our results suggest that NA stalk truncation or deglycosylation can be the pathogenic determinants of seasonal influenza viruses associated with the evolutionary adaptation of IAVs.
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