ArticlemBio2019
Low Polymerase Activity Attributed to PA Drives the Acquisition of the PB2 E627K Mutation of H7N9 Avian Influenza Virus in Mammals.
Article in mBio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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60 citing papers in PubMed, 85 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
- Syrian hamster is a valuable animal model for evaluating the transmissibility of emerging influenza viruses.Emerging microbes & infections · 2026Article
- Outbreak of H9N2 avian influenza viruses in lesser rhea in Peru, June-July 2025.bioRxiv : the preprint server for biology · 2026Article
- Characterization of emerging H3N3 avian influenza viruses in poultry in China.Emerging microbes & infections · 2025Article
- Epidemiology, evolution, and biological characteristics of avian influenza A (H11) viruses from wild birds.Virulence · 2025Article
- Cattle H5N1 outbreak in US driven by cow's "cross-nursing" behaviour: elucidating a novel transmission mechanism.Emerging microbes & infections · 2025Article
- Isoleucine at position 137 of haemagglutinin acts as a mammalian adaptation marker of H9N2 avian influenza virus.Emerging microbes & infections · 2025Article
- H5N1 virus invades the mammary glands of dairy cattle through 'mouth-to-teat' transmission.National science review · 2025Article
- A Review of Cross-Species Transmission Mechanisms of Influenza Viruses.Veterinary sciences · 2025Review
- Emergence of a novel reassortant H3N3 avian influenza virus with enhanced pathogenicity and transmissibility in chickens in China.Veterinary research · 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
- Proteomic Analysis of Differentially Expressed Proteins in A549 Cells Infected with H9N2 Avian Influenza Virus.International journal of molecular sciences · 2025Article
- PA and PA-X: two key proteins from segment 3 of the influenza viruses.Frontiers in cellular and infection microbiology · 2025Review
- Epidemiology and biological characteristics of influenza A (H4N6) viruses from wild birds.Emerging microbes & infections · 2024Article
- Amino acid mutations PB1-V719M and PA-N444D combined with PB2-627K contribute to the pathogenicity of H7N9 in mice.Veterinary research · 2024Article
- BAG6 inhibits influenza A virus replication by inducing viral polymerase subunit PB2 degradation and perturbing RdRp complex assembly.PLoS pathogens · 2024Article
- Wild Bird-Origin H6N2 Influenza Virus Acquires Enhanced Pathogenicity after Single Passage in Mice.Viruses · 2024Article
- Article
- Avian ANP32A incorporated in avian influenza A virions promotes interspecies transmission by priming early viral replication in mammals.Science advances · 2024Article
- Alarming situation of emerging H5 and H7 avian influenza and effective control strategies.Emerging microbes & infections · 2023Review
Corrections and comments
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Authors and funding
23 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Avian influenza viruses (AIVs) must acquire mammalian-adaptive mutations before they can efficiently replicate in and transmit among humans. The PB2 E627K mutation is known to play a prominent role in the mammalian adaptation of AIVs. The H7N9 AIVs that emerged in 2013 in China easily acquired the PB2 E627K mutation upon replication in humans. Here, we generate a series of reassortant or mutant H7N9 AIVs and test them in mice. We show that the low polymerase activity attributed to the viral PA protein is the intrinsic driving force behind the emergence of PB2 E627K during H7N9 AIV replication in mice. Four residues in the N-terminal region of PA are critical in mediating the PB2 E627K acquisition. Notably, due to the identity of viral PA protein, the polymerase activity and growth of H7N9 AIV are highly sensitive to changes in expression levels of human ANP32A protein. Furthermore, the impaired viral polymerase activity of H7N9 AIV caused by the depletion of ANP32A led to reduced virus replication in
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