Duck plague virus gG is secreted, nonstructural glycoprotein, not essential for viral replication and responsible for the virulence.

Abstract

Duck plague virus (DPV) is a highly pathogenic member of the herpesvirus family that can induce significant morbidity and mortality, primarily manifesting as septicemia in multiple host organs. The US4 gene encodes glycoprotein gG, which is highly conserved across the alphaherpesvirus family. To date, our laboratory has conducted preliminary bioinformatics analysis and prokaryotic expression studies of DPV US4; however, there is a paucity of literature regarding its biological characteristics and functions. In this study, we demonstrated that the DPV US4 gene encodes gG, a nonstructural glycoprotein that is present in infected cells and is secreted into the supernatant. Additionally, gG was found to interact with the duck chemokines CXCL8 and CCL26. To elucidate the role of gG in DPV pathogenesis, both in vitro and in vivo experiments were conducted. The in vitro data revealed that expression of the gG protein had no significant effect on any stage of the viral life cycle, suggesting that gG is not essential for viral replication. In vivo studies demonstrated that ducks infected with the gG-knockout virus presented minimal organ lesions and a significantly lower mortality rate than did those infected with the wild-type virus. Furthermore, gG modulated the transcription levels of host interferons, proinflammatory cytokines, and chemokines. This study elucidates the role of gG in DPV pathogenesis and provides a theoretical foundation for further investigations into the potential function of gG in modulating the host immune response.