ArticleNature communications2023
An Influenza A virus can evolve to use human ANP32E through altering polymerase dimerization.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Mapping in-cell protein contact sites reveals hijacking of paraspeckles during influenza A virus infection.Nature microbiology · 2026Article
- Divergent pathogenic mechanisms of influenza A and influenza B viruses.Archives of microbiology · 2026Review
- The emergence and molecular evolution of H5N1 influenza viruses in United States dairy cattle.bioRxiv : the preprint server for biology · 2026Article
- Advancing immunity and disease resistance in chickens through genome editing.Journal of animal science and biotechnology · 2026Review
- 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
- The potential of H5N1 viruses to adapt to bovine cells varies throughout evolution.Nature communications · 2025Article
- Decoding non-human mammalian adaptive signatures of 2.3.4.4b H5N1 to assess its human adaptive potential.Microbiology spectrum · 2025Article
- ANP32 proteins from ticks and vertebrates are key host factors for replication of Bourbon virus across species.Journal of virology · 2025Article
- H5N1 2.3.4.4b: a review of mammalian adaptations and risk of pandemic emergence.The Journal of general virology · 2025Review
- Machine learning assessment of zoonotic potential in avian influenza viruses using PB2 segment.BMC genomics · 2025Article
- The global H5N1 influenza panzootic in mammals.Nature · 2025Review
- Understanding Influenza.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Abortive Infection of Animal Cells: What Goes Wrong.Annual review of virology · 2024Review
- 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
- Avian Influenza Virus A(H5Nx) and Prepandemic Candidate Vaccines: State of the Art.International journal of molecular sciences · 2024Review
- Rapid adaptive evolution of avian leukosis virus subgroup J in response to biotechnologically induced host resistance.PLoS pathogens · 2024Article
- Cryo-EM structures of Thogoto virus polymerase reveal unique RNA transcription and replication mechanisms among orthomyxoviruses.Nature communications · 2024Article
- Structures of H5N1 influenza polymerase with ANP32B reveal mechanisms of genome replication and host adaptation.Nature communications · 2024Article
- The host RNA polymerase II C-terminal domain is the anchor for replication of the influenza virus genome.Nature communications · 2024Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Human ANP32A and ANP32B are essential but redundant host factors for influenza virus genome replication. While most influenza viruses cannot replicate in edited human cells lacking both ANP32A and ANP32B, some strains exhibit limited growth. Here, we experimentally evolve such an influenza A virus in these edited cells and unexpectedly, after 2 passages, we observe robust viral growth. We find two mutations in different subunits of the influenza polymerase that enable the mutant virus to use a novel host factor, ANP32E, an alternative family member, which is unable to support the wild type polymerase. Both mutations reside in the symmetric dimer interface between two polymerase complexes and reduce polymerase dimerization. These mutations have previously been identified as adapting influenza viruses to mice. Indeed, the evolved virus gains the ability to use suboptimal mouse ANP32 proteins and becomes more virulent in mice. We identify further mutations in the symmetric dimer interface which we predict allow influenza to adapt to use suboptimal ANP32 proteins through a similar mechanism. Overall, our results suggest a balance between asymmetric and symmetric dimers of influenza virus polymerase that is influenced by the interaction between polymerase and ANP32 host proteins.
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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.