ArticleVirology2016
1918 Influenza receptor binding domain variants bind and replicate in primary human airway cells regardless of receptor specificity.
Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Intra-patient neuraminidase mutations in avian H5N1 influenza virus reduce sialidase activity to complement weaker hemagglutinin binding and facilitate human infection.PLoS pathogens · 2026Article
- The pathogenesis of influenza in intact alveoli: virion endocytosis and its effects on the lung's air-blood barrier.Frontiers in immunology · 2024Review
- Relevance of Host Cell Surface Glycan Structure for Cell Specificity of Influenza A Viruses.Viruses · 2023Article
- The 1918 Influenza Pandemic and Its Legacy.Cold Spring Harbor perspectives in medicine · 2020Review
- Fifty Years of Influenza A(H3N2) Following the Pandemic of 1968.American journal of public health · 2020Article
- Alternative Experimental Models for Studying Influenza Proteins, Host-Virus Interactions and Anti-Influenza Drugs.Pharmaceuticals (Basel, Switzerland) · 2019Review
- The 1918 influenza pandemic: 100 years of questions answered and unanswered.Science translational medicine · 2019Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The 1918 influenza pandemic caused ~50 million deaths. Many questions remain regarding the origin, pathogenicity, and mechanisms of human adaptation of this virus. Avian-adapted influenza A viruses preferentially bind α2,3-linked sialic acids (Sia) while human-adapted viruses preferentially bind α2,6-linked Sia. A change in Sia preference from α2,3 to α2,6 is thought to be a requirement for human adaptation of avian influenza viruses. Autopsy data from 1918 cases, however, suggest that factors other than Sia preference played a role in viral binding and entry to human airway cells. Here, we evaluated binding and entry of five 1918 influenza receptor binding domain variants in a primary human airway cell model along with control avian and human influenza viruses. We observed that all five variants bound and entered cells efficiently and that Sia preference did not predict entry of influenza A virus to primary human airway cells evaluated in this model.
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Registered trials
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