Skip to main content
. 2020 Feb 14;9(1):366–377. doi: 10.1080/22221751.2020.1725398

Figure 7.

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.