Figure 7.
A model of the mechanism by which DHX9 attenuates the restriction of HBV replication by A3B. HBV infection induces upregulation of DHX9 by inhibiting its proteasome-dependent degradation mediated by MDM2, as demonstrated previously [20], then the upregulated DHX9 interacts with A3B and attenuates the binding of A3B with HBV pgRNA. As a consequence, DHX9 suppresses the anti-HBV function of A3B to promote viral replication.