ArticleScientific reports2017
Prerequisites for the acquisition of mammalian pathogenicity by influenza A virus with a prototypic avian PB2 gene.
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 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Rule-based meta-analysis reveals the major role of PB2 in influencing influenza A virus virulence in mice.BMC genomics · 2019Pooled it
- Emergence of Novel Reassortant H3N2 Avian Influenza Viruses in Southern China: Genetic Complexity and Pathogenicity in Chickens and Mice.Animals : an open access journal from MDPI · 2026Article
- Genetic Optimization of Early 2009 Pandemic H1N1 Vaccine Strains for Improved Replication in Embryonated Chicken Eggs.Journal of microbiology and biotechnology · 2025Article
- Evolutionary trajectories and zoonotic potential of a PB2 mutation triad (I147T, K339T, and A588T) in avian influenza viruses.Veterinary research · 2025Article
- Development of an H9N2 vaccine strain with enhanced neuraminidase immunogenicity via dual hemagglutinin and neuraminidase modification.Journal of veterinary science · 2025Article
- Article
- A High-Yield Recombinant Inactivated Whole-Virion Nasal Influenza A(H1N1)pdm09 Virus Vaccine with an Attenuated PB2 Gene.International journal of molecular sciences · 2025Article
- Intranasally administered whole virion inactivated vaccine against clade 2.3.4.4b H5N1 influenza virus with optimized antigen and increased cross-protection.Virology journal · 2025Article
- Characterization of highly pathogenic avian influenza A (H5N1) viruses isolated from cats in South Korea, 2023.Emerging microbes & infections · 2024Article
- Exploring Potential Intermediates in the Cross-Species Transmission of Influenza A Virus to Humans.Viruses · 2024Review
- Engineering an Optimal Y280-Lineage H9N2 Vaccine Strain by Tuning PB2 Activity.International journal of molecular sciences · 2023Article
- A Novel Triple Reassortment H3N8 Avian Influenza Virus: Characteristics, Pathogenicity, and Transmissibility.Transboundary and emerging diseases · 2023Article
- Highly pathogenic avian influenza (A/H5N1) virus outbreaks in Lesotho, May 2021.Emerging microbes & infections · 2022Article
- Selection of an Optimal Recombinant Egyptian H9N2 Avian Influenza Vaccine Strain for Poultry with High Antigenicity and Safety.Vaccines · 2022Article
- Whole-Genome Sequence Approach and Phylogenomic Stratification Improve the Association Analysis of Mutations With Patient Data in Influenza Surveillance.Frontiers in microbiology · 2022Article
- Article
- Parallel evolution in the emergence of highly pathogenic avian influenza A viruses.Nature communications · 2020Article
- An optimized molecular method for detection of influenza A virus using improved generic primers and concentration of the viral genomic RNA and nucleoprotein complex.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2019Article
- Acquisition of Innate Inhibitor Resistance and Mammalian Pathogenicity During Egg Adaptation by the H9N2 Avian Influenza Virus.Frontiers in microbiology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The polymerase of avian influenza A virus (AIV) is a heterotrimer composed of PB2, PB1, and PA. PB2 plays a role in overcoming the host barrier; however, the genetic prerequisites for avian PB2 to acquire mammalian pathogenic mutations have not been well elucidated. Previously, we identified a prototypic avian PB2 that conferred non-replicative and non-pathogenic traits to a PR8-derived recombinant virus when it was used to infect mice. Here, we demonstrated that key amino acid mutations (I66M, I109V, and I133V, collectively referred to as MVV) of this prototypic avian PB2 increase the replication efficiency of recombinant PR8 virus carrying the mutated PB2 in both avian and mammalian hosts. The MVV mutations caused no weight loss in mice, but they did allow replication in infected lungs, and the viruses acquired fatal mammalian pathogenic mutations such as Q591R/K, E627K, or D701N in the infected lungs. The MVV mutations are located at the interfaces of the trimer and are predicted to increase the strength of this structure. Thus, gaining MVV mutations might be the first step for AIV to acquire mammalian pathogenicity. These results provide new insights into the evolution of AIV in birds and mammals.
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