BST2 inhibits type I IFN (interferon) signaling by accelerating MAVS degradation through CALCOCO2-directed autophagy

Figures & data

Figure 1. A working model to illustrate a negative feedback loop of DDX58-mediated type I IFN signaling generated by a BST2-MARCH8-MAVS-CALCOCO2 axis. The transcription of the BST2 gene is upregulated once type I IFN signaling is activated. BST2 works as a virus restriction factor by tethering the virus particles in the infected cells. Meanwhile, BST2 recruits the E3 ubiquitin ligase MARCH8 to catalyze the K27-linked ubiquitination of MAVS at K7. Through recognition of K27-linked polyubiquitin chains on MAVS, CALCOCO2 delivers MAVS to phagophores for subsequent degradation, which shuts down the sustained activation of TBK1-IRF3 signaling in a negative feedback loop.