ArticlePLoS pathogens2020
Mutation of the second sialic acid-binding site of influenza A virus neuraminidase drives compensatory mutations in hemagglutinin.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Integrin β3 α2,6-sialylation by the sialyltransferase ST6Gal1 promotes human cytomegalovirus entry into fibroblasts.Virulence · 2026Article
- Genome-informed structural analysis of polymerase and glycoprotein adaptation in H5N1 clade 2.3.4.4b.Journal of veterinary science · 2026Article
- On the brink of emergence: an evolutionary approach to Influenza A virus H5N1 isolated from humans.Virus research · 2026Article
- MF59-adjuvanted A/Astrakhan influenza vaccine induces cross-neutralizing H5N1 antibodies in ferrets against circulating clade 2.3.4.4b viruses.NPJ vaccines · 2026Article
- The hemagglutinin proteins of clades 1 and 2.3.4.4b H5N1 highly pathogenic avian influenza viruses exhibit comparable attachment patterns to avian and mammalian tissues.Journal of virology · 2025Article
- Construction and Research Progress of Animal Models and Mouse Adapted Strains of Seasonal Influenza Virus.Vaccines · 2025Review
- Impact of naturally occurring hemagglutinin substitutions on antigenicity and fitness of influenza A(H5N1) virus.Npj viruses · 2025Article
- Molecular Evolution of the H5 and H7 Highly Pathogenic Avian Influenza Virus Haemagglutinin Cleavage Site Motif.Reviews in medical virology · 2025Review
- Unraveling dynamics of paramyxovirus-receptor interactions using nanoparticles displaying hemagglutinin-neuraminidase.PLoS pathogens · 2024Article
- Molecular Markers and Mechanisms of Influenza A Virus Cross-Species Transmission and New Host Adaptation.Viruses · 2024Review
- Heteromultivalent Ligand Display on Reversible Self-Assembled Monolayers (rSAMs): A Fluidic Platform for Tunable Influenza Virus Recognition.ACS applied materials & interfaces · 2024Article
- Recurring incursions and dissemination of novel Eurasian-origin H5Nx avian influenza viruses in Atlantic Canada.Virus evolution · 2024Article
- Receptor Binding Properties of Neuraminidase for influenza A virus: An Overview of Recent Research Advances.Virulence · 2023Review
- Compensatory mutations in the matrix protein of viral hemorrhagic septicemia virus (VHSV) genotype IVa in response to artificial mutation of two amino acids (D62A E181A).Virus research · 2023Article
- Letter to the editor: Highly pathogenic influenza A(H5N1) viruses in farmed mink outbreak contain a disrupted second sialic acid binding site in neuraminidase, similar to human influenza A viruses.Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2023Article
- Preventing Influenza A Virus Infection by Mixed Inhibition of Neuraminidase and Hemagglutinin by Divalent Inhibitors.Journal of medicinal chemistry · 2022Article
- Next-generation T cell-activating vaccination increases influenza virus mutation prevalence.Science advances · 2022Article
- Influenza A Virus Neuraminidase Inhibitors.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Few Amino Acid Mutations in H6 Influenza A Virus From South American Lineage Increase Viral Replication Efficiency in Poultry.Frontiers in microbiology · 2022Article
- Second sialic acid-binding site of influenza A virus neuraminidase: binding receptors for efficient release.The FEBS journal · 2021Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A viruses (IAVs) cause seasonal epidemics and occasional pandemics. Most pandemics occurred upon adaptation of avian IAVs to humans. This adaptation includes a hallmark receptor-binding specificity switch of hemagglutinin (HA) from avian-type α2,3- to human-type α2,6-linked sialic acids. Complementary changes of the receptor-destroying neuraminidase (NA) are considered to restore the precarious, but poorly described, HA-NA-receptor balance required for virus fitness. In comparison to the detailed functional description of adaptive mutations in HA, little is known about the functional consequences of mutations in NA in relation to their effect on the HA-NA balance and host tropism. An understudied feature of NA is the presence of a second sialic acid-binding site (2SBS) in avian IAVs and absence of a 2SBS in human IAVs, which affects NA catalytic activity. Here we demonstrate that mutation of the 2SBS of avian IAV H5N1 disturbs the HA-NA balance. Passaging of a 2SBS-negative H5N1 virus on MDCK cells selected for progeny with a restored HA-NA balance. These viruses obtained mutations in NA that restored a functional 2SBS and/or in HA that reduced binding of avian-type receptors. Importantly, a particular HA mutation also resulted in increased binding of human-type receptors. Phylogenetic analyses of avian IAVs show that also in the field, mutations in the 2SBS precede mutations in HA that reduce binding of avian-type receptors and increase binding of human-type receptors. Thus, 2SBS mutations in NA can drive acquisition of mutations in HA that not only restore the HA-NA balance, but may also confer increased zoonotic potential.
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