Figure 8.

Diagram showing the proposed mechanism by which PRKAA/AMPK inhibits HBV production through promotion of autophagosome degradation. (A) Under normal conditions, AMPK is activated in response to HBV replication-induced production of cellular ROS. The activated AMPK promotes autophagic degradation and restricts the production of HBV. (B) Upon treatment with AMPK activator, increased activity of AMPK elevates the cellular ATP levels, leading to the promotion of autophagic degradation and elimination of HBV production.