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Abstract
Avian reoviruses are causative agents of tenosynovitis and viral arthritis. Historically, vaccination with live attenuated and inactivated vaccines provided protection against vertical transmission in breeders and by providing maternal antibodies to progeny. Since 2011, the incidence of tenosynovitis has increased dramatically and commercial vaccines no longer provide adequate protection against the variant viruses emerging from clinical cases. The reovirus outer-capsid attachment protein, σC, contains neutralizing epitopes and is the target for molecular characterization by genotyping. There are currently at least seven genotypes recognized and each genotype contains multiple subgroups. The commercially available vaccines make up a sub-group within genotype one. Reovirus field isolates are now commonly included in custom made inactivated vaccines, but the duration of immunity provided by the inactivated custom vaccines in the absence of an antigenically homologous live prime is unknown. We carried out three studies to evaluate antibody responses and an attenuation method to address the inadequacy of commercial vaccines to provide protection against variants. In the first investigation, the antibody response was evaluated following vaccination with a combination of commercial live attenuated/inactivated and/or a custom-made Genotype 5 vaccine. In the absence of a heterologous or homologous live prime, the antibody responses were significantly reduced compared either group that received the commercial live vaccine. In the second investigation, a variant pathogenic field isolate was attenuated by cold passage in a cell line and evaluated for pathogenicity. The cold-adapted virus was less pathogenic in day-old broiler chicks compared to the parent virus isolate. Results from this study provide evidence that cold-adaptation of avian reovirus variants in a cell line is suitable for a more rapid method of attenuation. In the third investigation, linear B-cell epitope mapping was performed on a commercial vaccine and two variants in order to identify the molecular basis behind the antigenic differences of commercial live vaccines and variants. Fewer B-cell epitopes within σC were observed in birds that received only live or inactivated vaccinations. For both of the variant viruses, a combination of live and inactivated vaccinations resulted in the most complex B-cell response to σC. Identification of the antibody binding sites on σC advances the understanding of how variant reoviruses escape vaccine-induced protection, and this information will enhance diagnostic evaluations, vaccine design, and vaccine selection.