[Infection with hepatitis B virus enhances basal autophagy]

Hepatitis B virus (HBV) is a major human pathogen that chronically infects 400 million people worldwide. Chronic infection of HBV plays a key role in the pathogenesis of cirrhosis and hepatocellular carcinoma (HCC). To clarify the mechanism of HBV-related HCC and immune escape of HBV, we investigated the relationship between infection of HBV and basal autophagy.

To examine the number of autophagosomes upon transfection with HBV, HepG2.2.15 cells were transfected with green fluorescent protein-microtubule-associated protein 3 (GFP-LC3) and observed by fluorescence microscopy. Huh7 or HepG2 cells was transiently transfected with HBV expression vector pHBV1.3, then the phosphatidylethanol-amine conjugation of microtubule-associated protein 3 (LC3) and the degradation of p62, both of which are specific indictors of autophagy,were evaluated by western blot. Moreover, HepG2 or Chang liver cells were transiently transfected with the constructed HBV X protein ( HBx) expression vector in order to evaluate autophagic status of the cells.

HBV and HBx were both able to increase the autophagosomes formation as well as the enhancement of autophagic flux. Notably, C type HBx had a more increment of autophagy than B type does.

HBV can enhance basal autophagy and the increment is dependent on HBx. Different genotypes of HBx had different effects on basal autophagy. Take together, these findings will help us to clarify the mechanism of HBV infection and the development of Hepatitis B to HCC in the future study.