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Immediate PB2-E627K amino acid substitution after single infection of highly pathogenic avian influenza H5N1 clade 2.3.4.4b in mice

Kim et al., Virology Journal, doi:10.1186/s12985-025-02811-w, Jun 2025
https://c19early.org/kim26.html
Mouse study showing rapid gain-of-function adaptation of an avian H5N1 virus with lethal disease (100% mortality at a 4:1 challenge-to-contact ratio) and efficient contact transmission in BALB/c mice.
Kim et al., 5 Jun 2025, China, peer-reviewed, 5 authors. Contact: songcs@konkuk.ac.kr, donghunlee@konkuk.ac.kr.
Immediate PB2-E627K amino acid substitution after single infection of highly pathogenic avian influenza H5N1 clade 2.3.4.4b in mice
Deok-Hwan Kim, Dong-Yeop Lee, Yeram Seo, Chang-Seon Song, Dong-Hun Lee
Virology Journal, doi:10.1186/s12985-025-02811-w
The H5N1 subtype of highly pathogenic avian influenza (HPAI) virus, first identified in a goose in Guangdong, China, in 1996 (Gs/GD), has since spread globally, infecting various domestic and wild bird species and occasionally crossing the species barrier to infect mammals, including humans [1] . In autumn 2020, novel reassortant clade 2.3.4.4b H5N1 HPAI viruses were detected and became predominant among poultry and wild birds in Europe, subsequently spread to Africa, the Middle East, and Asia [2] . Since then, numerous mammalian infections have been reported worldwide in species such as black bears, bobcats, coyotes, and ferrets. Most cases were
Author contributions Declarations Ethics approval and consent to participate All experiments involving viable HPAI H5N1 viruses were conducted in Biosafety Level 3 (BSL-3) facilities at Konkuk University, following procedures approved by the Konkuk University Institutional Biosafety Committee (approval no. KUIBC-2024-06). Animal infection studies were reviewed, approved, and supervised by the Institutional Animal Care and Use Committee of Konkuk University (approval no. KU24080). Consent for publication Not applicable. Competing interests The authors declare no competing interests. Publisher's note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
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Alexakis, Buczkowski, Ducatez, Fusaro, Gonzales et al., Avian influenza overview June-September 2024, Efsa J, doi:10.2903/j.efsa.2024.9057
Bauer, Benavides, Kroeze, De, Van Riel, The neuropathogenesis of highly pathogenic avian influenza H5Nx viruses in mammalian species including humans, Trends Neurosci, doi:10.1016/j.tins.2023.08.002
Boivin, Hart, Interaction of the influenza A virus polymerase PB2 C-terminal region with importin alpha isoforms provides insights into host adaptation and polymerase assembly, J Biol Chem, doi:10.1074/jbc.M110.182964
Bortz, Westera, Maamary, Steel, Albrecht et al., Host-and strain-specific regulation of influenza virus polymerase activity by interacting cellular proteins, mBio, doi:10.1128/mBio.00151-11
Briggs, Kapczynski, Comparative analysis of PB2 residue 627E/K/V in H5 subtypes of avian influenza viruses isolated from birds and mammals, Front Vet Sci, doi:10.3389/fvets.2023.1250952
Charostad, Zadeh Rukerd, Mahmoudvand, Bashash, Hashemi et al., A comprehensive review of highly pathogenic avian influenza (HPAI) H5N1: an imminent threat at doorstep, Travel Med Infect Dis, doi:10.1016/j.tmaid.2023.102638
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Massin, Van Der Werf, Naffakh, Residue 627 of PB2 is a determinant of cold sensitivity in RNA replication of avian influenza viruses, J Virol, doi:10.1128/jvi.75.11.5398-5404.2001
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Wan, Lessons from emergence of A/goose/Guangdong/1996-like H5N1 highly pathogenic avian influenza viruses and recent influenza surveillance efforts in Southern China, Zoonoses Public Health
Zhang, Zhao, Guo, Zhang, Li et al., Amino acid substitutions associated with avian H5N6 influenza A virus adaptation to mice, Front Microbiol, doi:10.3389/fmicb.2017.01763
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