Monkeypox is an emerging zoonotic disease with a growing prevalence outside of its endemic area, posing a significant threat to public health. Despite the epidemiological and field investigations of monkeypox, little is known about its maintenance in natural reservoirs, biological implications or disease management. African rodents are considered possible reservoirs, although many mammalian species have been naturally infected with the monkeypox virus (MPXV). The involvement of domestic livestock and pets in spillover events cannot be ruled out, which may facilitate secondary virus transmission to humans. Investigation of MPXV infection in putative reservoir species and non-human primates experimentally uncovered novel findings relevant to the course of pathogenesis, virulence factors and transmission of MPXV that provided valuable information for designing appropriate prevention measures and effective vaccines.

Reovirus infections in turkeys are associated with arthritis and lameness. Viral genome sequence data are scarce, which makes an accurate description of the viral evolution and epidemiology difficult. In this study, we isolated and characterized turkey reoviruses from Hungary. The isolates were identified in 2016; these isolates were compared with earlier Hungarian turkey reovirus strains and turkey reoviruses isolated in the 2010s in the United States. Gene-wise sequence and phylogenetic analyses identified the cell-receptor binding protein and the main neutralization antigen, σC, to be the most conserved. The most genetically diverse gene was another surface antigen coding gene, μB. This gene was shown to undergo frequent reassortment among chicken and turkey origin reoviruses. Additional reassortment events were found primarily within members of the homologous turkey reovirus clade. Our data showed evidence for low variability among strains isolated from independent outbreaks, a finding that suggests a common source of turkey reoviruses in Hungarian turkey flocks. Given that commercial vaccines are not available, identification of the source of these founder virus strains would permit a more efficient prevention of disease outbreaks before young birds are settled to fattening facilities.

The concern that the vaccines currently used against Avian orthoreovirus (ARV) infections are less efficient in the field justifies the need for the close monitoring of circulating ARV strains. In this study, we collected necropsy samples from various chicken breeds and tested for ARV by virus isolation, RT-PCR assay and sequence analysis. ARVs were isolated from birds showing runting-stunting syndrome, uneven growth, lameness or increased mortality, with relative detection rates of 38%, 35%, 6% and 25%, respectively. Partial σC gene sequences were determined for nearly 90% of ARV isolates. The isolates could be classified into one of the major genetic clusters. Interestingly, cluster 2 and cluster 5 were isolated from vaccinated broiler breeders, while clusters 1 to 4 were isolated from unvaccinated broilers. The isolates shared less than 75% amino acid identities with the vaccine strains (range, 44.3–74.6%). This study reaffirms the global distribution of the major genetic clusters of ARVs in chicken. The diversity of ARV strains isolated from unvaccinated broilers was greater than those detected from vaccinated animals, however, the relative importance of passive and active immunity on the selection of novel strains in different chicken breeds needs to be better understood.

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.