ArticleJournal of virology2023
Mammalian ANP32A and ANP32B Proteins Drive Differential Polymerase Adaptations in Avian Influenza Virus.
Article in Journal of virology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 50 citations in OpenAlex.
- The mouse-lethal H5N1 influenza virus carrying the PB2-384L/443R/460M characteristics acquired in avian hosts can effectively utilize human ANP32A/B proteins.Emerging microbes & infections · 2026Article
- Acidic nuclear phosphoprotein 32A (ANP32A): structure, function, and its role in disease pathogenesis.Molecular biology reports · 2026Review
- Divergent pathogenic mechanisms of influenza A and influenza B viruses.Archives of microbiology · 2026Review
- Host-Directed Antiviral Strategies Against Influenza Viruses: Host Targets, Multi-Omics Approaches and AI-Assisted Discovery.Veterinary sciences · 2026Review
- Pathogenicity and immune response of turkey A(H1N2) influenza virus of swine-origin on turkeys and mice.Veterinary research · 2026Article
- On the brink of emergence: an evolutionary approach to Influenza A virus H5N1 isolated from humans.Virus research · 2026Article
- Historical Pandemic and Contemporary Influenza A Viruses Reveal PB2 M631L as a Convergent Adaptation to Human ANP32.Microorganisms · 2026Article
- The emergence and molecular evolution of H5N1 influenza viruses in United States dairy cattle.bioRxiv : the preprint server for biology · 2026Article
- Enhanced genome replication activity of pandemic H1N1 influenza A virus through PA mutations.Journal of virology · 2026Article
- Adaptation differences and mechanisms of influenza viruses to ANP32 proteins across species.Journal of virology · 2026Review
- Polymerase mutations underlie early adaptation of H5N1 influenza virus to dairy cattle and other mammals.Nature communications · 2026Article
- Article
- Confronting the known unknown: historical lessons and future strategies for Disease X.Frontiers in public health · 2026Review
- H5N1 clade 2.3.2.1e lineage transition in Lao PDR during 2023-2024 associated with regional spread and human infection risk-associated receptor-binding features.Frontiers in public health · 2026Article
- Evolution, spread and impact of highly pathogenic H5 avian influenza A viruses.Nature reviews. Microbiology · 2026Review
- Influenza virus research in an era of emerging respiratory threats: host-virus interactions, surveillance technologies, antiviral management and resistance, and vaccine preparedness.Frontiers in microbiology · 2026Review
- Transboundary Spread and Ecological Drivers of HPAI H5N1 Clade 2.3.4.4b During the 2022-2023 Outbreak in Chile: An Integrated Genomic and Spatial Epidemiology Framework.Transboundary and emerging diseases · 2026Article
- Emergence of mammalian-adaptive PB2 mutations enhances polymerase activity and pathogenicity of cattle-derived H5N1 influenza A virus.Nature communications · 2025Article
- The potential of H5N1 viruses to adapt to bovine cells varies throughout evolution.Nature communications · 2025Article
- Evolutionary trajectories and zoonotic potential of a PB2 mutation triad (I147T, K339T, and A588T) in avian influenza viruses.Veterinary research · 2025Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
ANP32 proteins, which act as influenza polymerase cofactors, vary between birds and mammals. In mammals, ANP32A and ANP32B have been reported to serve essential but redundant roles to support influenza polymerase activity. The well-known mammalian adaptation PB2-E627K enables influenza polymerase to use mammalian ANP32 proteins. However, some mammalian-adapted influenza viruses do not harbor this substitution. Here, we show that alternative PB2 adaptations, Q591R and D701N, also allow influenza polymerase to use mammalian ANP32 proteins, whereas other PB2 mutations, G158E, T271A, and D740N, increase polymerase activity in the presence of avian ANP32 proteins as well. Furthermore, PB2-E627K strongly favors use of mammalian ANP32B proteins, whereas D701N shows no such bias. Accordingly, PB2-E627K adaptation emerges in species with strong pro-viral ANP32B proteins, such as humans and mice, while D701N is more commonly seen in isolates from swine, dogs, and horses, where ANP32A proteins are the preferred cofactor. Using an experimental evolution approach, we show that the passage of viruses containing avian polymerases in human cells drove acquisition of PB2-E627K, but not in the absence of ANP32B. Finally, we show that the strong pro-viral support of ANP32B for PB2-E627K maps to the low-complexity acidic region (LCAR) tail of ANP32B.
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