Table 1.

Mechanisms of HBV-mediated autophagic responses.

HBV Proteins.	Models	Mechanisms	Effects	References
HBx	HepG2.2.15 and HepAD38 cells	Activate AMPK by ROS accumulation	Induce autophagy initiation (?)	[14]
			Promote autophagic degradation
HBx	Primary rat hepatocytes; HepG2.2.15 cells and primary hepatocytes	Activate AMPK signaling	Induce autophagy initiation	[34,36]
HBx	L02, Chang, HepG2, and BEL-7404 cells	Directly transactivates BECN1 promoter activity and upregulates its expression during starvation	Promote phagophore formation	[11]
HBx	Chang cells	Increase the activity of DAPK in a BECN1-associated pathway	Promote phagophore formation	[12]
SHBs	Huh7 cells	Activate IRE1α/XBP1/BECN1 axis	Promote phagophore formation	[13,37]
HBx	Huh7.5 cells	Directly bind to PtdIns3K and enhance its enzymatic activity	Promote phagophore formation	[38]
HBx	HepG2 cells	Dissociate BECN1 and Bcl-2 via the ROS/JNK signaling pathway	Promote phagophore formation	[39]
HBx	HepG2.2.15 and Huh7 cells; primary human hepatocytes; hydrodynamic-based HBV mouse model	Activate BECN1-mediated autophagy through C-myc/miR-192-3p/XIAP/NF-κB axis	Promote phagophore formation	[40]
SHBs	Huh7 cells	Activate PERK/eIF2α and ATF6/GRP78/94 signaling to enhance their interaction with the autophagy-associated proteins ATG5, ATG12, and/or ATG16L	Activate phagophore expansion and form autophagosomes	[13,37]
HBx	Huh7 cells	Impair lysosome maturation by inhibiting its acidification	Interfere with autophagic degradation	[16]
HBV	HepG2.2.15 and Huh7 cells	Block the fusion of autophagosomes with lysosomes by decreasing the expression of Rab7 and SNAP29	Interfere with autophagic degradation	[18,21,41]