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Isolation and characterization of an Aves polyomavirus 1 from diseased budgerigars in China

Ma, Jingjiao, Wu, Rujuan, Tian, Ye, Zhang, Min, Wang, Weili, Li, Yujie, Tian, Fulin, Cheng, Yuqiang, Yan, Yaxian, Sun, Jianhe
Veterinary microbiology 2019
Aves polyomavirus 1, amino acid substitution, bird diseases, brain, breeding, budgerigars, consensus sequence, genome, genotype, heart, in vitro studies, innate immunity, interferon-beta, intestines, liver, nucleotide sequences, pathogenicity, phylogeny, proteins, viral load, China, Poland
Aves polyomavirus 1 (APV) causes inflammatory disease in psittacine birds, especially in young budgerigar. In this study, an APV virus (SD18 strain) was isolated from a diseased psittacine birds breeding facility. The full genome (4981 bp) of SD18 was determined and analyzed. Phylogenetic analysis of full genome sequences indicated all the APV strains form two groups. The SD18 strain showed close relationship with APV isolated from Poland, however, the other Chinese strains are located in group II, which suggested different genotypes APVs are co-circulating in China. Compared with the consensus sequence of APV full genome, the SD18 strain contains 13 nucleotide mutations, and 2 unique amino acid substitutions (R179 M and Q382 K) located in VP2/3 and Large T proteins. To explore the pathogenicity of the virus, the SD18 strain was used to challenge 2-week-old budgerigars. All infected birds died no later than 5 days post infection, and virus was detected in multiple organs including brain, heart, ingluvies, liver, and intestine, which indicated that SD18 is fatal and causes systemic infection in young budgerigar. In vitro studies showed that SD18 replicated efficiently in CEF cells and reached the highest viral titers at 9 days post infection. Notably, replication of SD18 stimulated IFN-β response in CEF cells and overexpression of the VP4 or VP4Delta proteins significantly inhibited IFN-β promoter activation, which could be the strategy of APV to escape from the host innate immunity.