Abstract
Avian reoviruses have been isolated from chickens with a variety of disease conditions. The most important of these is tenosynovitis (viral arthritis) where a rela- tionship between the virus and disease has been established. The present thesis investigated some aspects of the patho- genesis of experimental reovirus infection in chickens.
The first part of the work describes the standardiza- tion of immunohistochemical techniques including immunofluo- rescence and immunoperoxidase staining for tracing virus in tissues as a basis for later later pathogenesis studies. In addition, an indirect enzyme-linked immunosorbent assay was developed to measure reovirus antibody titres in a single dilution of serum.
Early events in reovirus pathogenesis were studied by virological, immunohistochemical and electron microscopic methods. These showed viral entry and primary replication in the epithelium of the intestine and bursa of Fabricius within 12 hours following following oral infection. These were followed by a rapid pantropic distribution of virus which reached most tissues within 24 to 48 hours after infection.
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Following infection of day-old chicks by different routes, cloacal virus shedding continued for about to 4 weeks and virus persisted in hock (tibiotarsal- tarsometatarsal) joints until the end of the experiment (5 weeks). Although the isolation of virus from the joint was often difficult in the later stages of infection, joint lesions still continued to progress. When compared with oral or subcutaneous infection, direct inoculation of virus into the hock joint or foot-pad enhanced the disease process with the development of cartilage lesions as early as 2 to 3 weeks after infection.
Young chicks infected at 1-day of age did not serocon- vert until 2 to 3 weeks later, but in mature chickens antibodies were detected as early as 1 week post-infection. Chickens infected at 1-day of age developed a delayed- type hypersensitivity reaction at 6 weeks of age following challenge with viral antigen. Maternal antibodies appeared to protect newly-hatched chicks against reovirus infection by preventing viral spread to target tissues, although primary replication in the intestine was unaffected.
Preliminary studies provided evidence for the develop- ment of autoantibodies, such as antinuclear and anti- collagen antibodies antibodies following reovirus infection, but rheumatoid factor was not detected. Immune complexes were present in the sera of infected chickens.
The evidence from this study supported the proposal that reovirus-induced arthritis chickens could
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be a valuable model for rheumatoid and other forms of chronic arthritis with particular reference to investigation of the pathogenesis of synovial injury associated with infection or allergy.