Immunopathogenesis of avian leukosis virus subgroup J in white leghorn chickens

Avian leukosis virus subgroup J (ALV-J) was first described in the early 1990s in England as the cause of myeloid leukosis. Since its discovery, the virus is now spread worldwide and broiler breeder companies are trying to rid their breeder flocks of the infection. Accidental infection has also occurred in commercial laying chickens. The overall goal of this research was to determine the pathogenesis of ALV-J infection in white leghorn chickens. The objectives were: (1) Compare the pathogenicity of ALV-J in various lines of white leghorn chickens; (2) Determine the effects of endogenous virus 21 on the pathogenesis of ALV-J in white leghorns; and (3) Determine the tissue tropism of ALV-J and the susceptibility of the B cell to ALV-J induced transformation in white leghorns.; For objective 1, chickens from four genetic lines of white leghorn were inoculated with the U.S. prototype of ALV-J, ADOL Hc1, at either the day of hatch or as 7-day-old embryos. At 4, 10, 20 and 30 weeks of age, chickens were tested for ALV-J-induced viremia and antibody, packed cell volumes, and differential white blood cell counts. At 4 and 10 weeks of age, 5 chickens from each treatment group and of each line were humanely euthanized and bursal tissues were examined for follicle transformation. All birds that died and those that survived the experiment were examined for tumor formation. Microscopic examination of the grossly affected tissues also was performed to confirm the diagnosis of tumors. Of all the lines of chickens inoculated with ALV-J at day of hatch, only Line 0 developed antibodies and cleared the virus. Chickens of all other lines had various degrees of success in developing antibody and clearing the virus. The primary tumors observed were lymphoid leukosis (LL) and hemangiomas, regardless of treatment or genetic line of chicken.; For objective 2, the effect of endogenous leukosis virus 21 (EV21) on the pathogenesis of ALV-J induced infection and disease was examined. F1 progeny from a cross between ADOL line 0.44-EV21+ males and ADOL 15B₁ females were hatched and characterized as late feathering or early feathering by the length of the primary feathers. Chicks were inoculated with strain ADOL Hc1 of ALV-J at day of hatch. At 4, 10, 18 and 31 weeks of age, chickens were tested for ALV-J viremia and antibody. All birds that died and those that survived the experiment were necropsied. Chickens harboring EV21 mounted a weak antibody response as compared with those lacking EV21. Although the incidence of tumors was surprisingly low for birds harboring EV21, overall LL was diagnosed in five birds and hemangioma in one bird.; Tissue tropism and B cell transformation assays were studied in chickens of line 15I₅ X 7₁, a highly susceptible line to ALV-induced infection and tumors. Chicks were inoculated as 7-day-old embryos with strain ADOL Hc1 of ALV-J. At 2 and 6 weeks of age, various tissues were tested by immunohistochemistry utilizing a monoclonal antibody specific for gp85. Viral antigen was found in all tissues examined except skeletal muscle. At 4 and 10 weeks of age, bursal tissues were examined for the presence of transformed follicles using the methyl green pyronine stain. Results indicated that ALV-J could transform bursal follicles. Infection with ALV-J may be manifested as LL.