ArticleScience advances2024
Effect of pandemic influenza A virus PB1 genes of avian origin on viral RNA polymerase activity and pathogenicity.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed.
- Fever as thermal barrier: avian‑origin PB1 enables influenza A viruses to overcome mammalian febrile defense.Signal transduction and targeted therapy · 2026Article
- PB1 mutations as key drivers of influenza A virus evolution.Frontiers in microbiology · 2026Review
- Innate immune role of IL-6 in influenza a virus pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- The phylogenetic, pathogenicity and transmission capacity analysis of one H9N2 strain.Frontiers in veterinary science · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zoonotic influenza A virus (IAV) infections pose a substantial threat to global health. The influenza RNA-dependent RNA polymerase (RdRp) comprises the PB2, PB1, and PA proteins. Of the last four pandemic IAVs, three featured avian-origin PB1 genes. Prior research linked these avian PB1 genes to increased viral fitness when reassorted with human IAV genes. This study evaluated chimeric RdRps with PB1 genes from the 1918, 1957, and 1968 pandemic IAVs in a low pathogenic avian influenza (LPAI) virus background to assess polymerase activity and pathogenicity. Substituting in the pandemic PB1 genes reduced polymerase activity, virulence, and altered lung pathology, while the native LPAI PB1 showed the highest pathogenicity and polymerase activity. The native LPAI PB1 virus caused severe pneumonia and high early viral RNA levels, correlating with elevated host cytokine signaling. Increased genetic distance from the LPAI PB1 sequence correlated with reduced polymerase activity, IFN-β expression, viral replication, and pathogenicity.
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