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An Ex Vivo Chicken Primary Bursal-cell Culture Model to Study Infectious Bursal Disease Virus Pathogenesis
Published on: October 4, 2018
Co-infection with CAV facilitates ALV-K replication and induces severe immunosuppression in chickens
Yuling Cui1, Mengyue Dong2, Zhanxin Wang3
1State Key Laboratory of Swine and Poultry Breeding Industry & Heyuan Branch, Guangdong Provincial Laboratory of Lingnan Modern Agricultural Science and Technology, College of Animal Science, South China Agricultural University, Guangzhou 510642, PR China; Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangzhou, Guangdong 510642, PR China; South China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou 510642, PR China; Guangdong Provincial Key Lab of AgroAnimal Genomics and Molecular Breeding, College of Animal Science, South China Agricultural University, Guangzhou 510642, PR China; Guangdong Engineering Research Center for Vector Vaccine of Animal Virus, Guangzhou 510642, PR China.
Abstract:
Avian leukosis virus subgroup K (ALV-K) and chicken anemia virus (CAV) are important immunosuppressive pathogens in poultry, and co-infection between these viruses is increasingly reported in field conditions. However, the pathogenic interactions between ALV-K and CAV remain poorly understood. In this study, specific pathogen-free (SPF) chickens were experimentally infected with ALV-K or CAV alone, or co-infected with both viruses, to evaluate their synergistic effects. This study systematically analyzed survival rate, growth performance, histopathological changes, immune organ indices, viral replication, and host immune responses. The results showed that co-infection significantly reduced survival rate and suppressed body weight gain compared with single infections. More severe pathological lesions were observed in the liver, spleen, kidney, and bursa of Fabricius in co-infected chickens. Notably, CAV infection significantly not only enhanced ALV-K replication in peripheral blood and multiple tissues but also prolonged viremia. Whereas, ALV-K did not affect CAV replication. In addition, co-infection induced marked immunological alterations, characterized by increased expression of pro-inflammatory and antiviral cytokines, including IL-6 and IFN-α, and a significant reduction in IFN-γ and IL-10. More importantly, co-infection also inhibited the proliferation and activation of peripheral CD4⁺ and CD8⁺ T lymphocytes. These findings demonstrate that CAV promotes ALV-K replication and aggravates disease severity by inducing immunosuppression and immune dysregulation, thereby contributing to the synergistic pathogenicity observed during co-infection. This study provides a basis for future studies aimed at elucidating the underlying mechanisms of viral co-infection and support the development of effective prevention and control strategies.
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