ArticleNature communications2019
Profiling host ANP32A splicing landscapes to predict influenza A virus polymerase adaptation.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Adaptation differences and mechanisms of influenza viruses to ANP32 proteins across species.Journal of virology · 2026Review
- Evolution, spread and impact of highly pathogenic H5 avian influenza A viruses.Nature reviews. Microbiology · 2026Review
- Emergence of mammalian-adaptive PB2 mutations enhances polymerase activity and pathogenicity of cattle-derived H5N1 influenza A virus.Nature communications · 2025Article
- ANP32 proteins from ticks and vertebrates are key host factors for replication of Bourbon virus across species.Journal of virology · 2025Article
- Chicken ANP32A-independent replication of highly pathogenic avian influenza viruses potentially leads to mammalian adaptation-related amino acid substitutions in viral PB2 and PA proteins.Journal of virology · 2025Article
- Human ANP32A/B are SUMOylated and utilized by avian influenza virus NS2 protein to overcome species-specific restriction.Nature communications · 2024Article
- Proximal protein landscapes of the type I interferon signaling cascade reveal negative regulation by PJA2.Nature communications · 2024Article
- PB2 residue 473 contributes to the mammalian virulence of H7N9 avian influenza virus by modulating viral polymerase activity via ANP32A.Journal of virology · 2024Article
- Avian ANP32A incorporated in avian influenza A virions promotes interspecies transmission by priming early viral replication in mammals.Science advances · 2024Article
- Equine ANP32 proteins support influenza A virus RNA polymerase activity.Virologica Sinica · 2023Article
- An Influenza A virus can evolve to use human ANP32E through altering polymerase dimerization.Nature communications · 2023Article
- The SUMO-interacting motif in NS2 promotes adaptation of avian influenza virus to mammals.Science advances · 2023Article
- Mammalian ANP32A and ANP32B Proteins Drive Differential Polymerase Adaptations in Avian Influenza Virus.Journal of virology · 2023Article
- Comparative analysis of PB2 residue 627E/K/V in H5 subtypes of avian influenza viruses isolated from birds and mammals.Frontiers in veterinary science · 2023Article
- Are pigs overestimated as a source of zoonotic influenza viruses?Porcine health management · 2022Review
- The C-terminal LCAR of host ANP32 proteins interacts with the influenza A virus nucleoprotein to promote the replication of the viral RNA genome.Nucleic acids research · 2022Article
- The Host Factor ANP32A Is Required for Influenza A Virus vRNA and cRNA Synthesis.Journal of virology · 2022Article
- Host Cell Factors That Interact with Influenza Virus Ribonucleoproteins.Cold Spring Harbor perspectives in medicine · 2021Review
- BRD9 is a druggable component of interferon-stimulated gene expression and antiviral activity.EMBO reports · 2021Article
- IFITM3 incorporation sensitizes influenza A virus to antibody-mediated neutralization.The Journal of experimental medicine · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Species' differences in cellular factors limit avian influenza A virus (IAV) zoonoses and human pandemics. The IAV polymerase, vPol, harbors evolutionary sites to overcome restriction and determines virulence. Here, we establish host ANP32A as a critical driver of selection, and identify host-specific ANP32A splicing landscapes that predict viral evolution. We find that avian species differentially express three ANP32A isoforms diverging in a vPol-promoting insert. ANP32As with shorter inserts interact poorly with vPol, are compromised in supporting avian-like IAV replication, and drive selection of mammalian-adaptive vPol sequences with distinct kinetics. By integrating selection data with multi-species ANP32A splice variant profiling, we develop a mathematical model to predict avian species potentially driving (swallow, magpie) or maintaining (goose, swan) mammalian-adaptive vPol signatures. Supporting these predictions, surveillance data confirm enrichment of several mammalian-adaptive vPol substitutions in magpie IAVs. Profiling host ANP32A splicing could enhance surveillance and eradication efforts against IAVs with pandemic potential.
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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.