Differential expression of transforming growth factor-β1 and HBx enhances hepatitis B virus replication and augments host immune cytokines and chemokines.

Background/Aims. This study investigated how HBV replication and host immune response are effected by reduced expression of TGF-β1 and HBx. Material and methods. Short interfering RNA (siRNA) knockdown technology has been used to examine the role of TGF-β1 in hepatitis B virus replication. The siTGF-β1 has been transfected along with 1.3mer HBV x-null to investigate the knockdown effect of TGF-β1 on HBV replication and host immune factors. Results. In this study, we found that diminished expression of TGF-β1 and increased expression of HBx enhances HBV replication several folds. The differential expression of TGF-β1 and HBx also stimulated transcriptional viral replicative intermediate (pgRNA) and secretion of core and ‘e’ antigen at translational level. Consequently, several cytokines such as IL-2, IL-8 and chemokine monocyte-chemoattractant protein (MCP-1) were increased significantly in response to stimulation of HBV replication. In contrast, TNF-α and RANTES mRNA expression increased insignificantly in response to enhanced HBV replication. Conclusions. We concluded that reduced expression of TGF-β1 together with HBx expression stimulate HBV replication and immune response, although the underlying mechanism of stimulation most likely differs.