Novel H10N3 avian influenza viruses have been frequently isolated from poultry across various regions of China (including Jiangsu, Zhejiang, Fujian, and other provinces) in recent years and have caused two cases of confirmed human infection.1, 2, 3 To prevent further human infection, an in-depth and systematic assessment of the pandemic risk of these viruses is essential. In this Correspondence, we report key findings from our investigation of the genomic and biological features of the H10N3 viruses isolated from humans and chickens.
An influenza A virus (A/Jiangsu/428/2021) was isolated from a 41-year-old man in China, representing the first recorded case of human infection with H10N3.1 During surveillance of live poultry markets in China from 2020 to 2022, we isolated 16 H10N3 viruses (appendix p 26). Phylogenetic analysis indicated that the haemagglutinin and neuraminidase genes belonged to the Eurasian lineage and formed a monophyletic group, suggesting a substantial evolutionary history of the novel H10N3 viruses before their detection (appendix pp 5, 11–12). The six internal genes originating from the H9N2 avian influenza A virus were grouped into multiple clusters and categorised into 15 genotypes (G0 to G14; appendix pp 5–6, 13–18, 33–34), suggesting that H10N3 viruses continue to evolve and undergo frequent reassortment. Such a persistent pattern of reassortment might enhance the fitness of avian influenza viruses in chickens and mammals, thereby posing a substantial threat to public health.
We identified multiple amino acid residues related to adaptation in mammalian hosts in these novel H10N3 viruses (appendix pp 6–7, 27–32), and both human-derived and chicken-derived isolates showed high affinity for sialic acid-α-2,6-galactose receptors (appendix pp 7, 19). The human-derived H10N3 virus can replicate at high frequencies in various mouse organs, displaying high pathogenicity in mice, with a median lethal dose of 1·2 log10 of the 50% egg infective dose (appendix pp 7–8, 20–22). Notably, the human-derived isolate was not transmitted to guinea pigs via respiratory droplets (appendix pp 9, 23–24). However, the chicken-derived virus CK/0132/21 was highly pathogenic to mice, with a median lethal dose of 3·2 log10 of the 50% egg infective dose, and could be transmitted between guinea pigs via respiratory droplets (appendix pp 7–9, 20–24). These results indicated that some chicken-derived viruses might hold the potential to evolve into a pandemic threat in the human population, without the need for prior adaptation.