ArticleScientific reports2016
Amino acid substitutions V63I or A37S/I61T/V63I/V100A in the PA N-terminal domain increase the virulence of H7N7 influenza A virus.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Pathogenicity, transmissibility, and receptor binding of a human-isolated influenza A (H10N5) virus.mBio · 2025Article
- Genetic Characterization of Kazakhstan Isolates: Avian Influenza H9N2 Viruses Demonstrate Their Potential to Infect Mammals.Viruses · 2025Article
- A low pathogenic avian influenza A/Mallard/South Korea/KNU2019-34/2019 (H1N1) virus has the potential to increase the mammalian pathogenicity.Virologica Sinica · 2025Article
- Mass Mortality in Terns and Gulls Associated with Highly Pathogenic Avian Influenza Viruses in Caspian Sea, Kazakhstan.Viruses · 2024Article
- Two amino acid residues in the N-terminal region of the polymerase acidic protein determine the virulence of Eurasian avian-like H1N1 swine influenza viruses in mice.Journal of virology · 2024Article
- High pathogenic avian influenza A(H5) viruses of clade 2.3.4.4b in Europe-Why trends of virus evolution are more difficult to predict.Virus evolution · 2024Article
- Pathogenicity and virulence of influenza.Virulence · 2023Review
- Vaccination and Antiviral Treatment against Avian Influenza H5Nx Viruses: A Harbinger of Virus Control or Evolution.Vaccines · 2023Review
- Hemagglutinin destabilization in H3N2 vaccine reference viruses skews antigenicity and prevents airborne transmission in ferrets.Science advances · 2023Article
- Global dissemination of H5N1 influenza viruses bearing the clade 2.3.4.4b HA gene and biologic analysis of the ones detected in China.Emerging microbes & infections · 2022Article
- Phylogenetic Inference of the 2022 Highly Pathogenic H7N3 Avian Influenza Outbreak in Northern Mexico.Pathogens (Basel, Switzerland) · 2022Article
- Article
- Swine H1N1 Influenza Virus Variants with Enhanced Polymerase Activity and HA Stability Promote Airborne Transmission in Ferrets.Journal of virology · 2022Article
- Characterization of H9N2 Avian Influenza Viruses Isolated from Poultry Products in a Mouse Model.Viruses · 2022Article
- An Outbreak of Highly Pathogenic Avian Influenza (H7N7) in Australia and the Potential for Novel Influenza A Viruses to Emerge.Microorganisms · 2021Review
- Generation of a pdmH1N1 2018 Influenza A Reporter Virus Carrying a mCherry Fluorescent Protein in the PA Segment.Frontiers in cellular and infection microbiology · 2021Article
- Risk of Environmental Exposure to H7N9 Influenza VirusFrontiers in cellular and infection microbiology · 2021Article
- Novel pathogenic characteristics of highly pathogenic avian influenza virus H7N9: viraemia and extrapulmonary infection.Emerging microbes & infections · 2020Article
- Full-length genome sequences of the first H9N2 avian influenza viruses isolated in the Northeast of Algeria.Virology journal · 2020Article
- HA stabilization promotes replication and transmission of swine H1N1 gamma influenza viruses in ferrets.eLife · 2020Article
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10 authors.
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Abstract
The PA N-terminal domain (PA-Nter) is essential for viral transcription and replication. Here we identified PA-Nter substitutions A37S, I61T, V63I and V100A in recently emerged avian influenza A viruses (IAVs) with potential effect on virus pathogenicity and/or host adaptation. We introduced the identified PA-Nter substitutions into avian H7N7 IAV by reverse genetics. Our results showed that single substitution V63I and combined substitutions, I61T/V63I and A37S/I61T/V63I/V100A (Mfour), significantly increased virus growth capacity in mammalian cells. Meanwhile, these substitutions conferred higher virus transcription/replication capacity by producing more mRNA, cRNA and vRNA. Consistently, the polymerase activity and the endonuclease activity were enhanced by these PA-Nter substitutions. Notably, substitutions V63I and Mfour strongly increased virus replication and virulence in mice. Collectively, our findings demonstrated that the PA-Nter substitutions V63I and Mfour enhanced IAV pathogenicity through modification of the polymerase activity and the endonuclease activity, which added to the evolving knowledge of IAV virulence determinants.
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