Chicken TAX1BP1 suppresses type I interferon production via degrading chicken MAVS and facilitates infectious bursal diseases virus replication

Abstract

Mammalian TAX1BP1 (TAX1 binding protein 1), originally identified as a partner of the HTLV-1 viral oncoprotein, functions in regulation of cellular cytokine production. TAX1BP1 plays an important signal transduction regulator, specifically modulating innate immune signaling pathways including NF–B and IRF3. The function of TAX1BP1, which regulates the innate immune response in mammals, has been well studied in previous reports, but the role of chicken TAX1BP1 (chTAX1) in IFN regulation and infectious bursal disease virus (IBDV) replication is still unclear. In this report, chTAX1 was successfully cloned and sub-inserted into a eukaryotic expression vector. The critical regions of chTAX1, such as LC3 binding motif, ubiquitin binding motif, are highly conserved compared to other organisms. We also found that chTAX1 inhibits IFN expression by promoting degradation of chicken MAVS (chMAVS). In addition, the distribution of chTAX1 altered and translocated to co-localize with both VP1 and VP3 after IBDV infection. Overexpression of chTAX1 promotes IBDV replication and knockdown of chTAX1 by RNA interference suppresses IBDV replication. In summary, our data initially indicate that chTAX1 is a suppressor of IFN expression as well as a promoter of IBDV replication.