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dc.contributor.authorStedman, Nancy Lisa
dc.date.accessioned2014-03-03T20:00:52Z
dc.date.available2014-03-03T20:00:52Z
dc.date.issued2001-05
dc.identifier.otherstedman_nancy_l_200105_phd
dc.identifier.urihttp://purl.galileo.usg.edu/uga_etd/stedman_nancy_l_200105_phd
dc.identifier.urihttp://hdl.handle.net/10724/20180
dc.description.abstractAvian leukosis viruses (ALV) are type C retroviruses that induce neoplasia, poor performance, cardiomyopathy, and immunosuppression in chickens. The novel ALV subgroup J (ALV-J) is a significant cause of myeloid neoplasia in broiler breeder chickens. Like subgroup B ALV, ALV-J has a strong tropism for monocytes and macrophages. Subgroup B ALV induce severe immunosuppression by inhibiting macrophage function. To investigate the impact of ALV-J infection on immune function, broiler chickens congenitally infected with ALV-J were produced from an infected breeder flock. Peripheral blood heterophils and peritoneal macrophages isolated from infected broilers exhibited no functional deficits in microbicidal and phagocytic ability relative to cells isolated from age- and breed-matched uninfected control chickens. ALV-J infected and uninfected chickens had similar heterophil functional enhancement and susceptibility to tenosynovitis and osteomyelitis after intravenous staphylococcal challenge. Macrophages from ALV-J infected chickens produced significantly more reactive nitrogen intermediates relative to those from uninfected chickens. ALV-J provirus was consistently detected by PCR in heterophils and macrophages isolated from infected chickens. Splenic mitogenic responses were similar for ALV-J infected and uninfected chickens. Thymus, cloacal bursa, and spleen were histologically similar in ALV-J infected and uninfected chickens. ALV-J infected chickens exhibited severe body weight suppression by 1 week of age that persisted throughout growout. ALV-J infected chickens had an 11% incidence of dilated cardiomyopathy whereas uninfected chickens had 0% incidence under identical conditions. In situ hybridization using an antisense riboprobe against ALV-J gp85 identified a strong viral tropism for myocardial and Purkinje fibers, pituitary and thyroid glands, and renal tubules and glomerular visceral epithelium. Intracytoplasmic viral inclusions were identified in myocardial and Purkinje fibers and glomerular visceral epithelium. The cardiac and endocrine tropism may relate pathogenetically to the cardiomyopathy and weight suppression in ALV-J infected broilers. Rarely ALV-J nucleic acid was identified in antigen presenting cells in immune organs, but not hematopoietic tissue. Despite the consistent detection of ALV-J provirus in heterophils and macrophages and rare detection of ALV-J nucleic acid in immune organs, no immune function deficits were identified in congenitally ALV-J infected broiler chickens. However, weight suppression and dilated cardiomyopathy are potentially economically important manifestations of ALV-J infection.
dc.publisheruga
dc.rightsOn Campus Only
dc.subjectAvian leukosis virus
dc.subjectAvian leukosis virus subgroup J
dc.subjectCardiomyopathy
dc.subjectChicken
dc.subjectHeterophil
dc.subjectImmunosuppression
dc.subjectIn situ hybridization
dc.subjectMacrophage
dc.subjectMitogenesis
dc.subjectPhagocytosis
dc.subjectReactive nitrogen intermediates
dc.subjectRetrovirus
dc.subjectStaphylococcus
dc.subjectWeight suppression
dc.titleAvian leukosis virus subgroup J
dc.title.alternativeeffects on immune function in broiler chickens
dc.typeDissertation
dc.description.degreePhD
dc.description.departmentPathology
dc.description.majorVeterinary Pathology
dc.description.advisorElizabeth Howerth
dc.description.committeeElizabeth Howerth
dc.description.committeeBarry Harmon
dc.description.committeeDenise Bounous
dc.description.committeeGeorge Rowland
dc.description.committeeMaricarmen Garcia


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