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Abstract
This research includes tissue tropism of avian leukosis virus subgroup J (ALV-J) in congenitally infected broiler chickens using an immunohistochemistry (IHC) technique detecting gp85 viral glycoprotein. All organs examined contained detectable antigen. The most intense staining was in the adrenal gland, heart, kidney, and proventriculus. Intense staining for viral antigen in the heart may explain the ability of ALVs to cause cardiomyopathy. Although recent investigations failed to demonstrate specific viral staining in bone marrow from infected chickens, this research shows moderate staining in myelocytic precursor cells in bone marrow. This agrees with previous work showing that cell cultures of bone marrow are susceptible to ALV-J infection, and the tendency of subgroup J to predominantly induce myeloid rather than lymphoid neoplasms. This research includes production of neutralization-resistant isolates of ALV-J. ADOL-7501 isolate of ALV-J was cloned in vitro by three serial terminal dilutions. The cloned virus was injected into specific pathogen free (SPF) chickens, and the antiserum produced had in vitro neutralizing activity against the cloned virus. The cloned virus was then serially passed three times in the presence of subneutralizing levels of this antiserum, and the resultant viral isolates were more resistant to antiserum neutralization in vitro than was the parent cloned virus. No nucleotide differences were detected between the env gene of the parent cloned virus and that of the neutralization-resistant mutants. Other possible genomic changes outside the env gene (i.e. in the LTR and gag genes) may account for these non-env based differences in neutralization indices. This research also includes an investigation of the protective effect of injected ALV-J antiserum in embryonated chickens eggs. In one experiment, chickens exposed to ALV-J by cohatching with virus-shedders did not suffer from body weight suppression or ALV related tumors, and the injected ALV-J antiserum did not protect against development of viremia or increase the number of chickens subsequently developing active immunity. In a second experiment, chickens were exposed to ALV-J by injection of virus at hatch. Injection of ALV-J antiserum protected these chickens against development of ALV-J related tumors, but did not protect against virus induced body weight suppression or development of viremia, and did not increase the number of chickens developing active immunity. In the third experiment, the protective effects of injecting antiserum against ALV-J into embryonating-chicken eggs before infection as embryos were determined by evaluating viremia, transfer of passive immunity, and localization of the virus in tissues from hatched chicks. The injected antiserum prevented viremia at hatch in four out of five chicks. Localization of ALV-J in chicks that were viremic at hatch was similar to previous investigations, with intense staining for viral antigen present in adrenal gland, heart, kidney, proventriculus, and spleen. Two of the chicks that were not viremic at hatch developed viremia at one week of age and had viral tissue distribution suggesting oral exposure to the virus from their hatchmate.