ArticlePLoS pathogens2013
Pandemic influenza A viruses escape from restriction by human MxA through adaptive mutations in the nucleoprotein.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.
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Who cites it
133 citing papers in PubMed, 204 citations in OpenAlex.
- Enhanced genome replication activity of pandemic H1N1 influenza A virus through PA mutations.Journal of virology · 2026Article
- Evolution, spread and impact of highly pathogenic H5 avian influenza A viruses.Nature reviews. Microbiology · 2026Review
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- The potential of H5N1 viruses to adapt to bovine cells varies throughout evolution.Nature communications · 2025Article
- High serological barriers may contribute to restricted Influenza-A-virus transmission between pigs and humans.One health (Amsterdam, Netherlands) · 2025Article
- Continuous evolution of Eurasian avian-like H1N1 swine influenza viruses with pdm/09-derived internal genes enhances pathogenicity in mice.Journal of virology · 2025Article
- Human MX1 orchestrates the cytoplasmic sequestration of neosynthesized influenza A virus vRNPs.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Molecular and ecological determinants of mammalian adaptability in avian influenza virus.Infection · 2025Review
- Viral interferon antagonism shapes host tropism.PLoS pathogens · 2025Review
- Genetic resilience or resistance in poultry against avian influenza virus: mirage or reality?Journal of virology · 2025Review
- An ancient influenza genome from Switzerland allows deeper insights into host adaptation during the 1918 flu pandemic in Europe.BMC biology · 2025Article
- Viral factors underlying the pandemic potential of influenza viruses.Microbiology and molecular biology reviews : MMBR · 2025Review
- Genetic diversity of H9N2 avian influenza viruses in poultry across China and implications for zoonotic transmission.Nature microbiology · 2025Article
- H5N1 2.3.4.4b: a review of mammalian adaptations and risk of pandemic emergence.The Journal of general virology · 2025Review
- Heterozygous and generalist MxA super-restrictors overcome breadth-specificity trade-offs in antiviral restriction.Science advances · 2025Article
- The evolution and epidemiology of H3N2 canine influenza virus after 20 years in dogs.Epidemiology and infection · 2025Article
- Exploring genetic signatures of zoonotic influenza A virus at the swine-human interface with phylogenetic and ancestral sequence reconstruction.Virus evolution · 2025Article
- The global H5N1 influenza panzootic in mammals.Nature · 2025Review
- Evolutionary dynamics and molecular epidemiology of H1N1 pandemic 2009 influenza A viruses across swine farms in Denmark.Virus evolution · 2025Article
- Replication Restriction of Influenza A(H5N1) Clade 2.3.4.4b Viruses by Human Immune Factor, 2023-2024.Emerging infectious diseases · 2025Article
73 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interferon-induced dynamin-like MxA GTPase restricts the replication of influenza A viruses. We identified adaptive mutations in the nucleoprotein (NP) of pandemic strains A/Brevig Mission/1/1918 (1918) and A/Hamburg/4/2009 (pH1N1) that confer MxA resistance. These resistance-associated amino acids in NP differ between the two strains but form a similar discrete surface-exposed cluster in the body domain of NP, indicating that MxA resistance evolved independently. The 1918 cluster was conserved in all descendent strains of seasonal influenza viruses. Introduction of this cluster into the NP of the MxA-sensitive influenza virus A/Thailand/1(KAN-1)/04 (H5N1) resulted in a gain of MxA resistance coupled with a decrease in viral replication fitness. Conversely, introduction of MxA-sensitive amino acids into pH1N1 NP enhanced viral growth in Mx-negative cells. We conclude that human MxA represents a barrier against zoonotic introduction of avian influenza viruses and that adaptive mutations in the viral NP should be carefully monitored.
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