Effects of cyclosporin A treatment on the pathogenesis of avian leukosis virus subgroup J infection in broiler chickens with Marek's disease virus exposure.
- Author:
Yongbaek KIM
1
;
Thomas P BROWN
;
Mary J PANTIN-JACKWOOD
Author Information
1. Department of Veterinary Pathology and Avian Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, USA. kim16@niehs.nih.gov
- Publication Type:Original Article
- Keywords:
Avian leukosis virus subgroup J;
cyclosporin A;
chickens
- MeSH:
Animals;
Antibodies, Viral/blood;
Avian Leukosis/*immunology/virology;
Avian leukosis virus/genetics/*immunology;
Body Weight;
*Chickens;
Cyclosporine/*pharmacology;
Dermatitis, Contact/immunology/virology;
Flow Cytometry;
Immunocompromised Host;
Immunohistochemistry/veterinary;
Immunophenotyping;
Immunosuppressive Agents/*pharmacology;
Lymphocyte Activation/immunology;
Marek Disease/*immunology/virology;
RNA, Viral/chemistry/genetics;
Reverse Transcriptase Polymerase Chain Reaction/veterinary;
T-Lymphocytes/*immunology/virology;
Viremia/veterinary
- From:Journal of Veterinary Science
2003;4(3):245-255
- CountryRepublic of Korea
- Language:English
-
Abstract:
In this study, we investigated the effects of T-cell suppression on the pathogenesis of subgroup J avian leukosis virus (ALV-J). Chickens were treated with cyclosporin A (CSP) 50 mg/Kg body weight or a corresponding volume of olive oil per every three days after hatching until the end of experiment. Some of the chickens from each treatment group were infected with an isolate of ALV-J, ADOL-7501, at 2 weeks of age. The effects of viral infection were compared to uninfected birds in same treatment group. Intramuscular injection of CSP induced significant T-cell specific immunosuppression determined by decreased cutaneous basophilic hypersensitivity response and decreased lymphocyte mitogenic activity using concanavalin A. Most of the chickens examined had Marek's disease virus infection prior to 3 weeks of age. The percentage of antibody-positive birds and antibody titers were similar in infected chickens between both treatment groups. The ratio of viremic chickens was significantly higher in CSP treated group than that of the Oil treated group. Microscopically, one CSP treated chicken had a nephroblastoma at 10 weeks post infection. At 7 and 10 weeks post-infection, more chickens had myeloid cell infiltrations in multiple organs including heart, liver and occasionally lung. Expression of ALV-J viral antigen determined by immunohistochemical staining was significantly higher in CSP treated chickens than Oil treated chickens at 10 weeks post-infection. This study indicated that chemically-induced T-cell suppression may enhance pathogenicity of the AVL-J virus in broilers.
