SGIV envelope protein VP088 facilitated virus replication via interacting with other viral proteins and promoting p62-dependent autophagic degradation of TBK1.

ABSTRACT: Singapore grouper iridovirus (SGIV), a novel member of the genus Ranavirus, family Iridoviridae, frequently causes a severe disease with high mortality in grouper aquaculture. Although previous findings have demonstrated that SGIV envelope protein VP088 was crucial for its infectivity, the underlying mechanism still remained uncertain. Here, we screened the potential viral proteins that interacted with VP088 during SGIV infection using GFP pull-down assay. Co-immunoprecipitation (Co-IP) assays verified the interactions between VP088 and VP018, VP068, or VP156 in vitro. Moreover, confocal microscopy analysis showed that VP088 markedly altered the cellular distribution of exogenously expressed VP018 and VP068 and ultimately translocated into virus assembly sites together upon S

SUBMITTER: Yuan M 

PROVIDER: S-EPMC12817895 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature