Abstract：
:The H9N2 influenza virus has been frequently endemic in poultry, infected mammals and humans and has threatened public health. It is therefore imperative to understand the molecular mechanism enabling this virus to jump from avian to mammalian species. In this study, two H9N2 influenza viruses were isolated from the same region in eastern China but from different hosts; one was isolated from mink and named A/Mink/Shandong/WM01/2014(H9N2)(WM01), while the other was isolated from chicken and named A/Chicken/Shandong/LX830/2014(H9N2)(LX830). Sequencing and phylogenetic analysis showed that both H9N2 influenza viruses had similar genetic backgrounds. The results of infection in minks suggested that both viruses caused significant weight loss and pathological changes in the lungs. Mouse infection showed that LX830 was nonpathogenic in mice, but WM01 resulted in 25% mortality and pathological changes in the lungs, such as severe edema and diffused inflammation of the interalveolar septa. Comparison of the full genomes of both H9N2 influenza viruses showed 52-nucleotide-synonym mutations in 8 gene segments and 7-nucleotide-antonym mutations, resulting in 7 amino acid (AA) substitutions distributed in the PB1, PA, NA and M gene segments. None of these mutations did affect splicing of the M and NS gene segments at the nucleotide level or minor open reading frames (ORFs), such as PB1-F2 and PA-X. Phylogenetic analysis showed that both H9N2 influenza viruses belong to the prevalent epidemic genotype in Asia. Keywords: H9N2 influenza virus; chicken; minks; pathogenicity; phylogenetic.
journal_name
Acta Viroljournal_title
Acta virologicaauthors
Ren W,Zhang CH,Li G,Liu G,Shan H,Li Jdoi
10.4149/av_2020_109subject
Has Abstractpub_date
2020-01-01 00:00:00pages
67-77issue
1eissn
0001-723Xissn
1336-2305journal_volume
64pub_type
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