ArticlePloS one2012
Mutations in polymerase genes enhanced the virulence of 2009 pandemic H1N1 influenza virus in mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 58 citations in OpenAlex.
- PA and PA-X: two key proteins from segment 3 of the influenza viruses.Frontiers in cellular and infection microbiology · 2025Review
- Amplicon sequencing of pasteurized retail dairy enables genomic surveillance of H5N1 avian influenza virus in United States cattle.PloS one · 2025Article
- Mutual antagonism of mouse-adaptation mutations in HA and PA proteins on H9N2 virus replication.Virologica Sinica · 2024Article
- Implications of the Immune Polymorphisms of the Host and the Genetic Variability of SARS-CoV-2 in the Development of COVID-19.Viruses · 2022Review
- Mutations in SARS-CoV-2 nsp7 and nsp8 proteins and their predicted impact on replication/transcription complex structure.Journal of medical virology · 2021Article
- Article
- The evolution and future of influenza pandemic preparedness.Experimental & molecular medicine · 2021Review
- Susceptibility of widely diverse influenza a viruses to PB2 polymerase inhibitor pimodivir.Antiviral research · 2021Article
- Structural and Thermodynamic Analysis of the Resistance Development to Pimodivir (VX-787), the Clinical Inhibitor of Cap Binding to PB2 Subunit of Influenza A Polymerase.Molecules (Basel, Switzerland) · 2021Article
- Diversity of SARS-CoV-2 isolates driven by pressure and health index.Epidemiology and infection · 2021Article
- PA Mutations Inherited during Viral Evolution Act Cooperatively To Increase Replication of Contemporary H5N1 Influenza Virus with an Expanded Host Range.Journal of virology · 2020Article
- A Single Amino Acid at Position 431 of the PB2 Protein Determines the Virulence of H1N1 Swine Influenza Viruses in Mice.Journal of virology · 2020Article
- Key Role of the Influenza A Virus PA Gene Segment in the Emergence of Pandemic Viruses.Viruses · 2020Review
- Article
- Pathogenicity of the H1N1 influenza virus enhanced by functional synergy between the NPV100I and NAD248N pair.PloS one · 2019Article
- Mutations in the H7 HA and PB1 genes of avian influenza a viruses increase viral pathogenicity and contact transmission in guinea pigs.Emerging microbes & infections · 2019Article
- Directed Evolution of an Influenza Reporter Virus To Restore Replication and Virulence and Enhance Noninvasive Bioluminescence Imaging in Mice.Journal of virology · 2018Article
- A Single Amino Acid in the Polymerase Acidic Protein Determines the Pathogenicity of Influenza B Viruses.Journal of virology · 2018Article
- Genetic and codon usage bias analyses of polymerase genes of equine influenza virus and its relation to evolution.BMC genomics · 2017Article
- The S128N mutation combined with an additional potential N-linked glycosylation site at residue 133 in hemagglutinin affects the antigenicity of the human H7N9 virus.Emerging microbes & infections · 2016Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Influenza A virus can infect a wide variety of animal species with illness ranging from mild to severe, and is a continual cause for concern. Genetic mutations that occur either naturally or during viral adaptation in a poorly susceptible host are key mechanisms underlying the evolution and virulence of influenza A virus. Here, the variants containing PA-A36T or PB2-H357N observed in the mouse-adapted descendants of 2009 pandemic H1N1 virus (pH1N1), A/Sichuan/1/2009 (SC), were characterized. Both mutations enhanced polymerase activity in mammalian cells. These effects were confirmed using recombinant SC virus containing polymerase genes with wild type (WT) or mutant PA or PB2. The PA-A36T mutant showed enhanced growth property compared to the WT in both human A549 cells and porcine PK15 cells in vitro, without significant effect on viral propagation in murine LA-4 cells and pathogenicity in mice; however, it did enhance the lung virus titer. PB2-H357N variant demonstrated growth ability comparable to the WT in A549 cells, but replicated well in PK15, LA-4 cells and in mice with an enhanced pathogenic phenotype. Despite such mutations are rare in nature, they could be observed in avian H5 and H7 subtype viruses which were currently recognized to pose potential threat to human. Our findings indicated that pH1N1 may adapt well in mammals when acquiring these mutations. Therefore, future molecular epidemiological surveillance should include scrutiny of both markers because of their potential impact on pathogenesis.
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