Glucocorticoid Stimulates Hepatitis B Viral Gene Expression in Cultured Human Hepatoma Cells

Open Access
Publisher Website
Google Scholar
Abstract
Glucocorticoids have been shown to influence the severity of hepatitis B virus-related chronic hepatitis in human. However, very little is known about the effects of glucocorticoids on hepatitis B virus replication in vitro. In this report, we used a welldifferentiated human hepatoma cell line, Hep3B, transfected with hepatitis B virus complementary DNA as a model to show that a glucocorticoid analog, dexamethasone, can directly stimulate the production of HBsAg and HBeAg. Elevation of 3.5–kb pregenomic RNA and all other viral RNAs in the transfected Hep3B cells after dexamethasone treatment supports the hypothesis that glucocorticoids directly stimulate hepatitis B virus gene expression in vitro. The concentration of dexamethasone for its half–maximal stimulatory activity toward HBsAg, HBeAg and all viral transcripts was approximately 10-8 mol/L, close to the affinity of glucocorticoid receptors to [3H]triamcinolone acetonide in Hep3B cells ( ± 10-8 mol/L). Specific glucocorticoid antagonist RU38486 completely blocked dexamethasone–induced HBV gene expression, suggesting that the stimulatory effect of dexamethasone was mediated through specific glucocorticoid receptors. (Hepatology 1992;16:13-18.)