ArticleJournal of virology2018
A Single Amino Acid in the Polymerase Acidic Protein Determines the Pathogenicity of Influenza B Viruses.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- A single mutation in nonstructural protein 1 is critical for the adaptive evolution of influenza B virus.Nature communications · 2026Article
- Genetic characterization and whole-genome sequencing-based genetic analysis of influenza B in Shandong Province during 2015-2024.Scientific reports · 2026Article
- Internal gene segments from a mouse-adapted influenza B virus confer increased pathogenicity to mice.PloS one · 2026Article
- Review
- N460S in PB2 and I163T in nucleoprotein synergistically enhance the viral replication and pathogenicity of influenza B virus.PLoS pathogens · 2025Article
- Identification of severity related mutation hotspots in SARS-CoV-2 using a density-based clustering approach.BioData mining · 2025Article
- Molecular characterisation of influenza B virus from the 2017/18 season in primary models of the human lung reveals improved adaptation to the lower respiratory tract.Emerging microbes & infections · 2024Article
- Genome characterization of influenza A and B viruses in New South Wales, Australia, in 2019: A retrospective study using high-throughput whole genome sequencing.Influenza and other respiratory viruses · 2024Article
- Genetic characterization and whole-genome sequencing-based genetic analysis of influenza virus in Jining City during 2021-2022.Frontiers in microbiology · 2023Article
- Expanding Mouse-Adapted Yamagata-like Influenza B Viruses in Eggs Enhances In Vivo Lethality in BALB/c Mice.Viruses · 2022Article
- Using amino acid features to identify the pathogenicity of influenza B virus.Infectious diseases of poverty · 2022Article
- Genome-wide association analysis of COVID-19 mortality risk in SARS-CoV-2 genomes identifies mutation in the SARS-CoV-2 spike protein that colocalizes with P.1 of the Brazilian strain.Genetic epidemiology · 2021Article
- A single N342D substitution in Influenza B Virus NA protein determines viral pathogenicity in mice.Emerging microbes & infections · 2020Article
- Characterization of Novel Cross-Reactive Influenza B Virus Hemagglutinin Head Specific Antibodies That Lack Hemagglutination Inhibition Activity.Journal of virology · 2020Article
- Reverse genetics for influenza B viruses and recent advances in vaccine development.Current opinion in virology · 2020Review
- Animal models for the risk assessment of viral pandemic potential.Laboratory animal research · 2020Review
- Comparative features of infections of two Massachusetts (Mass) infectious bronchitis virus (IBV) variants isolated from Western Canadian layer flocks.BMC veterinary research · 2018Article
- The phylogenomics of evolving virus virulence.Nature reviews. Genetics · 2018Review
- Restriction of H1N1 influenza virus infection by selenium nanoparticles loaded with ribavirin via resisting caspase-3 apoptotic pathway.International journal of nanomedicine · 2018Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza B virus (IBV) is one of the human respiratory viruses and one of the targets of seasonal vaccination. However, the bifurcation of two antigenically distinct lineages of IBVs makes it difficult to arrange proper medical countermeasures. Moreover, compared with pathogenicity-related molecular markers known for influenza A virus, little has been known for IBVs. To understand pathogenicity caused by IBVs, we investigated the molecular determinants of IBV pathogenicity in animal models. After serial lung-to-lung passages of Victoria lineage B/Brisbane/60/2008 (Vc_BR60) and Yamagata lineage B/Wisconsin/01/2010 (Ym_WI01) viruses in BALB/c mice, we identified the mouse-adapted Vc_BR60 (maVc_BR60) and Ym_WI01 (maYm_WI01) viruses, respectively. To find a molecular clue(s) to the increased pathogenicity of maVc_BR60 and maYm_WI01, we determined their genetic sequences. Several amino acid mutations were identified in the PB2, PB1, PA, BM2, and/or NS1 protein-coding regions, and one concurrent lysine (K)-to-arginine (R) mutation in PA residue 338 (PA K338R) was found in both maVc_BR60 and maYm_WI01 viruses. When analyzed using viruses rescued through reverse genetics, it was shown that PA K338R alone could increase the pathogenicity of both IBVs in mice and viral replication in the respiratory tracts of ferrets. In a subsequent minireplicon assay, the effect of PA K338R was highlighted by the enhancement of viral polymerase complex activity of both Vc_BR60 and Ym_WI01 viruses. These results suggest that the PA K338R mutation may be a molecular determinant of IBV pathogenicity via modulating the viral polymerase function of IBVs.
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