CHARACTERIZING BOVINE LEUKEMIA VIRUS INDUCED IMMUNOSUPRESSION IN ADULT NEW ZEALAND WHITE RABBITS(ORYCTOLAGUS CUNICULUS)
Open Access
- Graduate Program:
- Laboratory Animal Medicine
- Degree:
- Master of Science
- Document Type:
- Master Thesis
- Date of Defense:
- None
- Committee Members:
- Neil David Christensen, Thesis Advisor
- Xuwen Peng, Thesis Advisor
- Jiafen Hu, Thesis Advisor
- Timothy Cooper, Thesis Advisor
- Keywords:
- bovine leukemia virus
- immunosuppression
- Oryctolagus cuniculus
- lymphocyte subpopulations
- Abstract:
- Abstract A virus-induced immunosuppression model has yet to be fully described in the rabbit (Oryctolagus cuniculus). In this study we strive to characterize bovine leukemia virus (BLV) induced immunosuppression in the rabbit. BLV has been previously reported to induce persistent infection in rabbits resulting in an immunosuppression-like disease pathogenesis after a long (>12 months) incubation.1,2 This model will be valuable to study concurrent viral infection in human immunodeficiency virus (HIV)/ AIDS patients. The purpose of this study was to evaluate parameters and establish criteria for bovine leukemia virus (BLV)-induced immunosuppression in rabbits. Proviral DNA (pBLV913) or virus producing fetal lamb kidney cells (BLV-FLK) were used to initiate infection in rabbits over the course of 6 months. Peripheral blood lymphocytes were collected biweekly to quantitate helper T, cytotoxic T, and B lymphocyte populations using anti-CD4, anti-CD8, and anti-MHCII antibodies respectively. Serum samples were collected for detecting anti-BLV antibody generation by ELISA. Our results showed that, within the confines of the short observation period, BLV did not significantly alter the peripheral blood lymphocyte populations. BLV-FLK inoculation resulted in significant lower body weights in rabbits when compared with those in the control rabbits. All of the BLV-FLK cell-inoculated but none of the pBLV913-inoculated rabbits produced antibodies against BLV Gp51. Longer duration of study is needed to fully understand the pathogenesis of BLV in rabbits.