Infectious bursal disease virus (IBDV) infection still severely threatens the poultry industry, which needs more effective prevention and control measures. The tripartite motif proteins (TRIMs) play vital regulatory roles on virus replication and may be identified as potential targets. Therefore, we first employed high-throughput sequencing to screen and identify avian-derived TRIMs associated with IBDV infection and found that IBDV infection dramatically increased the expression level of TRIM71 in vivo and in vitro. These findings suggest that TRIM71 might be closely related to IBDV infection. Subsequently, the overexpression experiment showed that TRIM71 promoted IBDV replication, while knockdown of TRIM71 significantly inhibited IBDV replication. Mechanistically, TRIM71 interacted with the structural proteins VP1 and VP3. Besides, truncation assay showed that the NHL domain was the key domain for the interaction between TRIM71 and VP1, VP3. The study is the first to reveal that the avian-derived TRIM71 acts as a host proviral factor to promote IBDV replication by interacting with VP1 and VP3 depending on the NHL domain. Collectively, these findings not only provides a new insight into the interaction between IBDV and the host, but also provides a potential target for the development of novel prevention and control strategies.

Keywords: IBDV; NHL domain; Promote; TRIM71; VP1; VP3.