Bolin Hang1, Jianjun Sang2, Aijian Qin3, Kun Qian4, Hongxia Shao4, Mei Mei2, Jianqiang Ye4. 1. College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, PR China; College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang 453003, PR China. 2. College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, PR China. 3. College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, PR China; Jiangsu Co-innovation Centre for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, PR China. Electronic address: aijian@yzu.edu.cn. 4. College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, PR China; Jiangsu Co-innovation Centre for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, PR China.
Abstract
BACKGROUND: Avian leukosis virus subgroup J (ALV-J) causes tumours and immunosuppression in chickens. The host-ALV interactions at the transcriptional level are unknown. In this study, gene expression profiling was performed to analyse the bursa response induced by ALV-J strain JS09GY3 in chickens. RESULTS: A total of 594 gene transcripts displaying differential expression during ALV-J infection were identified. These differentially expressed genes are involved in binding, biological regulation, metabolic processes (MYF6 and FABP3), response to stimulus (F13A1 and CNGA3) and immune system processes (LY86, CATHL2, CCL4, and OASL), and several differentially expressed genes (e.g., ETV7, MMP9, and NOV) are involved in tumourigenesis. Eight differentially expressed genes were confirmed by quantitative reverse transcription-PCR (qRT-PCR). Based on pathway analysis, the notable signalling pathways mainly included cytokine-cytokine receptor interaction, the JAK-STAT signalling pathway and the RIG-1-like receptor signalling pathway. CONCLUSIONS: The gene expression profile obtained in this study may aid a better understanding of the molecular pathogenesis of ALV-J infection in chickens.
BACKGROUND:Avian leukosis virus subgroup J (ALV-J) causes tumours and immunosuppression in chickens. The host-ALV interactions at the transcriptional level are unknown. In this study, gene expression profiling was performed to analyse the bursa response induced by ALV-J strain JS09GY3 in chickens. RESULTS: A total of 594 gene transcripts displaying differential expression during ALV-J infection were identified. These differentially expressed genes are involved in binding, biological regulation, metabolic processes (MYF6 and FABP3), response to stimulus (F13A1 and CNGA3) and immune system processes (LY86, CATHL2, CCL4, and OASL), and several differentially expressed genes (e.g., ETV7, MMP9, and NOV) are involved in tumourigenesis. Eight differentially expressed genes were confirmed by quantitative reverse transcription-PCR (qRT-PCR). Based on pathway analysis, the notable signalling pathways mainly included cytokine-cytokine receptor interaction, the JAK-STAT signalling pathway and the RIG-1-like receptor signalling pathway. CONCLUSIONS: The gene expression profile obtained in this study may aid a better understanding of the molecular pathogenesis of ALV-J infection in chickens.