ArticleViruses2025
Progressive Adaptation of Subtype H6N1 Avian Influenza Virus in Taiwan Enhances Mammalian Infectivity, Pathogenicity, and Transmissibility.
Article in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Genomic characterization of H6N1 avian influenza viruses from wild birds and domestic ducks in the republic of Korea and Mongolia (2022-2024).Archives of virology · 2026Article
- A Novel Recombinant Chicken-Derived H6N8 Subtype Avian Influenza Virus Caused Disease in Chickens and Mice.Viruses · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The interspecies transmission of avian influenza viruses remains a significant public health concern. H6 viruses have gained attention following the first human infection by a chicken-origin H6N1 virus (A/Taiwan/02/2013, Hu/13), highlighting their zoonotic potential. To understand the evolutionary trajectory and mammalian adaptation of this Taiwan lineage, we compared two avian isolates (A/Chicken/Taiwan/CF19/2009, Ck/09; A/Chicken/Taiwan/2267/2012, Ck/12) and Hu/13 in vitro and in vivo. Hu/13 exhibited enhanced replication in MDCK cells, producing larger plaques and higher viral titers than Ck/09 and Ck/12. In BALB/c mice, Hu/13 demonstrated the highest pathogenicity and mortality, followed by Ck/12, while Ck/09 induced minimal morbidity. Hu/13 and Ck/12 replicated efficiently in respiratory tissues, eliciting robust cytokine responses and severe pulmonary lesions. In ferrets, Hu/13 showed relatively efficient transmission, infecting all direct physical-contact and two out of three airborne-contact ferrets, whereas Ck/09 failed to transmit. Histopathology confirmed escalating lung pathology from Ck/09 to Ck/12 and Hu/13. Whole-genome sequencing identified adaptive mutations in Hu/13 during ferret replication, though no canonical mammalian-adaptive changes (e.g., PB2-E627K or HA-Q226L) were detected. These findings demonstrate progressive mammalian adaptation, replication efficiency, and transmissibility within the Taiwan H6N1 lineage. Enhanced surveillance is crucial to monitor mammalian-adaptive mutations, informing pandemic preparedness and public health strategies.
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