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04 July 2018 : Laboratory Research  

Dexamethasone Stimulates Hepatitis B Virus (HBV) Replication Through Autophagy

Qiao He12E*, Xiaoyu Song1F, Yecai Huang3C, Wenjuan Huang2A, Bo Ye1B, Huaichao Luo1C, Hao Luo1C, Lichun Wu1B, Zuo Wang1D, Weixian Chen2A, Li Zhang1A

DOI: 10.12659/MSM.906250

Med Sci Monit 2018; 24: LBR4617-4624

Abstract

BACKGROUND: Reactivation of hepatitis B virus (HBV) is a fatal complication of chemotherapy. Occult HBV infection might be reactivated in patients undergoing chemotherapy or immunosuppression. However, the mechanism of HBV reactivation induced by chemotherapy or immunosuppression remains unclear.

MATERIAL AND METHODS: HepG2.2.15 cells were treated with an autophagy inducer (rapamycin), an inhibitor (3-methyladenine, 3-MA), and dexamethasone. Autophagosomes were observed by a transmission electron microscope (TEM). LC3-I, LC3-II, and P62 were analyzed by western blot. HBV replicative intermediates were detected by southern blot. HBV DNA expression was quantitated with real-time polymerase chain reaction (PCR). The level of HBV surface antigen (HBsAg) in culture medium was examined by ELISA.

RESULTS: In this study, we find that dexamethasone stimulates HBV replication and protein expression by inducing autophagy in HepG2.2.15 cells. In contrast, autophagy inhibitor (3-MA) abrogates HBsAg secretion stimulated by dexamethasone.

CONCLUSIONS: Our results suggest that dexamethasone stimulates HBV replication through autophagy. This might provide a novel insight into the mechanism of glucocorticoid-mediated HBV reactivation through autophagy, which might be a new therapeutic target.

Keywords: Dexamethasone, Hepatitis B virus

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Medical Science Monitor Basic Research eISSN: 2325-4416
Medical Science Monitor Basic Research eISSN: 2325-4416