Duck plague virus UL24 protein initiates K48/K63-linked IRF7 polyubiquitination to antagonize the innate immune response

Duck plague virus ( DPV ) is the pathogen of duck viral enteritis, which is highly infectious and can cause serious disease and death in ducks, geese and other waterfowl. Several envelope proteins of DPV have been shown to affect the cyclic GMP-AMP synthase ( cGAS ) -STING signaling pathway, thereby regulating the host 's innate immune response. DPV UL24 is an important DPV envelope protein that inhibits the activity of the IFN-β promoter. However, the mechanism of DPV UL24 protein regulating host innate immune response is still unclear. In this study, we found that DPV UL24 inhibited cGAS-STING and RIG-I/MDA5-MAVS signaling-mediated IFN-β activation. DPV UL24 reduced the mRNA expression of cGAS, STING, TBK1 and IRF7, and inhibited the protein expression of these factors. In addition, DPV UL24 induces K48 / k63-linked ubiquitination of IRF7 and promotes its degradation, thereby antagonizing the host innate immune response. The related research was published in the journal of poultry science with the title of ' Duck plague virus UL24 protein initiates K48 / K63-linked IRF7 polyubiquitination to the innate immune response '. https : / / doi : 10.1016 / j.psj.2024.104378.This study was supported by the China Agricultural Research System and MARA (CARS-42-17) of the Ministry of Agriculture and the Sichuan Veterinary Drug Innovation Research Group of the China Agricultural Research System (SCCXTD-2020-18).