Characterizing a newly identified avian herpesvirus-specific gene SORF3 in DPV and its roles in potential...

Duck plague virus (DPV) is a highly pathogenic avian herpesvirus that affects ducks, geese, and other anseriform poultry. The primary pathological changes observed in infected animals are mucosal, serosal, and systemic hemorrhages accompanied by exceptionally high fatality rates. While most DPV genes are conserved among herpesviruses, a small subset of genes, including the SORF3 gene, is unique to avian herpesviruses. To date, reports on the function and characteristics of the SORF3 gene are limited. In this study, the use of a polyclonal antibody against SORF3 demonstrated that this open reading frame could encode proteins. Through the use of DNA and protein synthesis inhibitors in infected cells, we delineated the gene's transcriptional and translational timeline, establishing SORF3 as a late gene. To further investigate the role of the protein encoded by the SORF3 gene in the pathogenic mechanism, we constructed a virus lacking the SORF3 gene. The growth kinetics results indicated that the SORF3 protein is not essential for viral replication. In vivo experimental findings revealed that while the SORF3-deleted virus still induced clinical symptoms and pathological changes associated with duck plague upon infection of ducks, its lethality was lower than that of the parental virus. In conclusion, this study revealed that the SORF3 gene, which is specific to avian herpesviruses, encodes a late viral protein in DPV and explored its potential role in DPV pathogenesis.IMPORTANCEDuck plague virus (DPV) has a high incidence rate and mortality rate of up to 90%, resulting in substantial economic losses in poultry farming. Consequently, investigating the temporal transcription and functional characterization of the proteins encoded by each DPV gene is crucial for understanding its complex life cycle and pathogenesis. This study revealed that the SORF3 gene, identified as an avian herpesvirus-specific gene, encodes a protein. Furthermore, the temporal transcription of this gene throughout the virus's life cycle confirmed that the protein encoded by SORF3 significantly influences the pathogenicity of DPV.