ArticleScientific reports2017
Replication of H9 influenza viruses in the human ex vivo respiratory tract, and the influence of neuraminidase on virus release.
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 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Dissecting the role of the HA1-226 leucine residue in the fitness and airborne transmission of an A(H9N2) avian influenza virus.Journal of virology · 2024Article
- Graphene oxide nanoparticles inhibit H9N2 influenza A virus infectivity by destroying viral coat proteins.Archives of virology · 2024Article
- Proposal for a Global Classification and Nomenclature System for A/H9 Influenza Viruses.Emerging infectious diseases · 2024Article
- Anti-hemagglutinin monomeric nanobody provides prophylactic immunity against H1 subtype influenza A viruses.PloS one · 2024Article
- Usp25-Erlin1/2 activity limits cholesterol flux to restrict virus infection.Developmental cell · 2023Article
- Review
- Leveraging 3D Model Systems to Understand Viral Interactions with the Respiratory Mucosa.Viruses · 2020Review
- Genetically and Antigenically Divergent Influenza A(H9N2) Viruses Exhibit Differential Replication and Transmission Phenotypes in Mammalian Models.Journal of virology · 2020Article
- Association of Increased Receptor-Binding Avidity of Influenza A(H9N2) Viruses with Escape from Antibody-Based Immunity and Enhanced Zoonotic Potential.Emerging infectious diseases · 2018Article
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
H9N2 viruses are the most widespread influenza viruses in poultry in Asia. We evaluated the infection and tropism of human and avian H9 influenza virus in the human respiratory tract using ex vivo respiratory organ culture. H9 viruses infected the upper and lower respiratory tract and the majority of H9 viruses had a decreased ability to release virus from the bronchus rather than the lung. This may be attributed to a weak neuraminidase (NA) cleavage of carbon-6-linked sialic acid (Sia) rather than carbon-3-linked Sia. The modified cleavage of N-acetlylneuraminic acid (Neu5Ac) and N-glycolylneuraminic acid (Neu5Gc) by NA in H9 virus replication was observed by reverse genetics, and recombinant H9N2 viruses with amino acids (38KQ) deleted in the NA stalk, and changing the amino acid at position 431 from Proline-to-Lysine. Using recombinant H9 viruses previously evaluated in the ferret, we found that viruses which replicated well in the ferret did not replicate to the same extent in the human ex vivo cultures. The existing risk assessment models for H9N2 viruses in ferrets may not always have a strong correlation with the replication in the human upper respiratory tract. The inclusion of the human ex vivo cultures would further strengthen the future risk-assessment strategies.
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