Avian leukosis virus subgroup J in broilers
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Avian leukosis virus subgroup J (ALV-J) infection causes significant economic loss because of increased mortality, tumor production, decreased production, and high costs for eradication. This research was performed to investigate the effects of immunosuppression on ALV-J pathogenesis. We developed RT-PCR based quantification methods for ALV-J RNA. The results of quantitiative competitive RT-PCR and real time RT-PCR based on a fluorogenic probe and SYBR Green I dye were strongly correlated to the TCID50s as determined by conventional culture methods. The new methods were also very specific, sensitive, relatively easy to perform, reproducible, and rapid compared with conventional culture methods.|The effects of the immunosuppression on ALV-J pathogenesis were determined in chickens with natural exposure to Marek’s disease virus. Suppression of B-cell and T-cell was induced by treatment of cyclophosphamide (CY) and cyclosporin A (CSP), respectively. Cyclophosphamide treatment induced significant B-lymphocyte suppression in broiler chickens throughout the experiment with transient effects on feather follicle epithelium, liver, kidney and bone marrow function. Chickens with immunosuppression of T- and B- cell function were more frequent ALV-J viremia with a higher virus titer compared to non-immunosuppressed groups. No significant difference in body weight gain was induced by ALV-J infection. While there were no neoplastic foci consistent with ALV-J infection in any of the control or CY-treated chickens, there was a nephroblastoma in a CSP treated chickens. Increased numbers of chickens in CSP treated groups had myeloid infiltrates compared to those present in control groups. This may indicate T-cell suppression increased tumor formation or preneoplastic myeloid proliferation in chickens with ALV-J infection. In immunohistochemical staining using monoclonal antibodies against ALV-J envelope glycoprotein, expression of the viral antigen was present in more chickens in the CY treated group compared to the control group at 3 weeks post-infection. With CSP treatment, the overall mean score of viral antigen expression was significantly higher compared to the control group at 10 weeks post-infection. With CY and CSP treatment, expression of viral antigen was significantly higher at 9 and 10 weeks post-infection at the end of the experiment compared to that present in 3 and 4 weeks post-infection, respectively.