UC Davis

Avian reoviruses are recognized for their genetic variability. The emergence of pathogenic variant strains causes negative impacts to the poultry industry worldwide. The disease prevention is based on the use of live classical and inactivated autogenous vaccines, however, they have a limited effect against the circulating variants, so they require a frequent update. The current molecular classification methods use the partial S1 gene that encodes the סC protein, but different genotypes do not always correlate with pathogenicity and sometimes induce a deficient cross-protection. Therefore, investigation of other variable genes and correlations between pathogenicity and antigenicity of variant strains is crucial for a better classification method. The present investigation focuses on the molecular, pathogenic, and antigenic characterization of emerging avian reovirus variant strains. This research is divided into three chapters. In the first chapter, we did a molecular characterization based on the S1 gene of 85 avian reoviruses obtained from the California outbreak and we did a whole-genome characterization of a portion of them. The characterized reoviruses were categorized in six genotypic clusters. We detected a shift in cluster representation throughout time occurred. According to the whole genome analyses, our results suggested that the L3, M2 and S1 genes accounted for most of the variability of these viruses. In chapter two we investigated the pathogenicity within the same S1 genotypic cluster variants. The genomes of two variant strains and a classical strain belonging to the same S1 genotype one were compared. Additionally, these strains were used in a challenge experiment involving inoculated and horizontally exposed specific-pathogen-free chickens. The whole-genome sequence analysis of the three strains revealed nucleotide identity differences in the L3, M2, and S1 genes. In addition, the variant strains indicated nucleotide identities differences in the S4 gene, despite having high homologies in all other genes. The challenge experiments showed that variant and classical strains replicated differently in tendons, hearts and duodena of the challenged and exposed chickens and caused dissimilar pathologic lesions and lymphoid depletion degrees in bursas and thymi of the challenged chickens. Because we consider that it is critical to associate genetic changes with the pathogenicity and antigenicity of variant strains in the selection of autogenous vaccines, in chapter three, we explored the association between the genetic and antigenic characteristics of 29 avian reoviruses, including conventional and variant strains using genetic and antigenic cartography. We detected high variation in terms of antigenicity which was not strongly correlated with the genetic composition of variable genes. The information generated in the present investigation contributes to the understanding of the epidemiology and pathobiology of avian reoviruses variant strains. In addition, it provides insights on how other genes besides S1 add variability in the diverse avian reovirus phenotypes.