ArticlePLoS pathogens2020
Selective usage of ANP32 proteins by influenza B virus polymerase: Implications in determination of host range.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 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
- Adaptation differences and mechanisms of influenza viruses to ANP32 proteins across species.Journal of virology · 2026Review
- 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
- ANP32 proteins from ticks and vertebrates are key host factors for replication of Bourbon virus across species.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
- 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
- Cryo-EM structures of Thogoto virus polymerase reveal unique RNA transcription and replication mechanisms among orthomyxoviruses.Nature communications · 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
- Existing Evidence for Influenza B Virus Adaptations to Drive Replication in Humans as the Primary Host.Viruses · 2023Review
- The SUMO-interacting motif in NS2 promotes adaptation of avian influenza virus to mammals.Science advances · 2023Article
- Article
- 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
- KPNA6 is a Cofactor of ANP32A/B in Supporting Influenza Virus Polymerase Activity.Microbiology spectrum · 2022Article
- Strategies targeting hemagglutinin cocktail as a potential universal influenza vaccine.Frontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The influenza B virus (IBV) causes seasonal influenza and has accounted for an increasing proportion of influenza outbreaks. IBV mainly causes human infections and has not been found to spread in poultry. The replication mechanism and the determinants of interspecies transmission of IBV are largely unknown. In this study, we found that the host ANP32 proteins are required for the function of the IBV polymerase. Human ANP32A/B strongly supports IBV replication, while ANP32E has a limited role. Unlike human ANP32A/B, chicken ANP32A has low support activity to IBV polymerase because of a unique 33-amino-acid insert, which, in contrast, exhibits species specific support to avian influenza A virus (IAV) replication. Chicken ANP32B and ANP32E have even lower activity compared with human ANP32B/E due to specific amino acid substitutions at sites 129-130. We further revealed that the sites 129-130 affect the binding ability of ANP32B/E to IBV polymerase, while the 33-amino-acid insert of chicken ANP32A reduces its binding stability and affinity. Taken together, the features of avian ANP32 proteins limited their abilities to support IBV polymerase, which could prevent efficient replication of IBV in chicken cells. Our results illustrate roles of ANP32 proteins in supporting IBV replication and may help to understand the ineffective replication of IBV in birds.
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