ArticleJournal of virology2012
Reassortment and mutation of the avian influenza virus polymerase PA subunit overcome species barriers.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 140 citations in OpenAlex.
- Regulatory hotspot on the influenza A virus polymerase revealed through the structure of the NEP-polymerase complex.Science advances · 2026Article
- Deep learning predicts potential reassortments of avian H5N1 with human influenza viruses.National science review · 2025Article
- Article
- Mammalian antiviral proteins ZAP and KHNYN can independently restrict CpG-enriched avian viruses.PLoS biology · 2025Article
- Mammalian ZAP and KHNYN can independently restrict CpG-enriched avian viruses.bioRxiv : the preprint server for biology · 2025Article
- Study on the Mechanism of RuHaoDaShi Granules in Treating H1N1 Viral Pneumonia Based on Network Pharmacology and Experimental Validation.Pathogens (Basel, Switzerland) · 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
- The biology of the avian influenza virus: A comprehensive review with insights into novel therapeutic strategies.Open veterinary journal · 2025Review
- Machine learning methods for predicting human-adaptive influenza A virus reassortment based on intersegment constraint.Frontiers in microbiology · 2025Article
- PA and PA-X: two key proteins from segment 3 of the influenza viruses.Frontiers in cellular and infection microbiology · 2025Review
- In silico prediction of pathogen's pandemic potential using the viral trait assessment for pandemics (ViTAP) model.PNAS nexus · 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
- Structures of influenza A and B replication complexes give insight into avian to human host adaptation and reveal a role of ANP32 as an electrostatic chaperone for the apo-polymerase.Nature communications · 2024Article
- Naturally occurring PAVirologica Sinica · 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
- An Influenza A virus can evolve to use human ANP32E through altering polymerase dimerization.Nature communications · 2023Article
- Viral vectored vaccines: design, development, preventive and therapeutic applications in human diseases.Signal transduction and targeted therapy · 2023Review
- Article
- A Novel Triple Reassortment H3N8 Avian Influenza Virus: Characteristics, Pathogenicity, and Transmissibility.Transboundary and emerging diseases · 2023Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The emergence of new pandemic influenza A viruses requires overcoming barriers to cross-species transmission as viruses move from animal reservoirs into humans. This complicated process is driven by both individual gene mutations and genome reassortments. The viral polymerase complex, composed of the proteins PB1, PB2, and PA, is a major factor controlling host adaptation, and reassortment events involving polymerase gene segments occurred with past pandemic viruses. Here we investigate the ability of polymerase reassortment to restore the activity of an avian influenza virus polymerase that is normally impaired in human cells. Our data show that the substitution of human-origin PA subunits into an avian influenza virus polymerase alleviates restriction in human cells and increases polymerase activity in vitro. Reassortants with 2009 pandemic H1N1 PA proteins were the most active. Mutational analyses demonstrated that the majority of the enhancing activity in human PA results from a threonine-to-serine change at residue 552. Reassortant viruses with avian polymerases and human PA subunits, or simply the T552S mutation, displayed faster replication kinetics in culture and increased pathogenicity in mice compared to those containing a wholly avian polymerase complex. Thus, the acquisition of a human PA subunit, or the signature T552S mutation, is a potential mechanism to overcome the species-specific restriction of avian polymerases and increase virus replication. Our data suggest that the human, avian, swine, and 2009 H1N1-like viruses that are currently cocirculating in pig populations set the stage for PA reassortments with the potential to generate novel viruses that could possess expanded tropism and enhanced pathogenicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.