Two avian reovirus strains (A and B) from clinically affected poultry flocks, belonging to the same genetic cluster based on a partial sequence of the sigmaC coding region, were compared for molecular and pathogenicity aspects including intra-host dissemination and inter-host transmission capabilities, microscopic lesions and viral load in different organs. Strain B caused a 10% mortality and more severe liver and heart lesions, with slower transmission to contact animals. In contrast, Strain A showed rapid transmission and lower pathogenicity, without mortality. Whole genome sequence analysis revealed mosaicism in both strains, with gene segments of vaccine-like or vaccine origin. High nucleotide and amino acid sequence identities were noted, except for the lambdaC, muB, and sigmaC genes. LambdaC gene of Strain B grouped with vaccine strains, whereas Strain A branched with wild-type reoviruses. The muB gene of Strain B resembled alleles found in some Hungarian and Chinese chicken-origin strains and a pheasant-origin reassortant. Despite similar S1 genes, the strains exhibited different pathogenicity and transmission abilities. These findings suggest that sigmaC-based genotyping can obscure pathogenicity differences. Whole genome sequencing and characterization are essential to identify molecular markers of pathogenicity, reinforced by a curated sequence and standardized pathogenicity database.Research highlights ARV strains of the same genotype had distinct pathogenic and transmission traits.( LambdaC, muB, and sigmaC genes made a difference. SigmaC-based genotyping obscures pathogenicity differences.
Kovács et al. (Wed,) studied this question.