FIG 7.
Proposed model for the interplay between TRIM25, RIG-I, and NS1-B. After influenza B virus infection, TRIM25-mediated RIG-I ubiquitination promotes the eruption of IFNs, ISGs, and proinflammatory factors. Host cells utilize TRIM25 to interact with the N-terminal RBD of NS1-B (N-NS1-B) and to relieve the inhibitory effect of the NS1-B C-terminal TED (C-NS1-B) on RIG-I ubiquitination.