Alpha- enolase regulates hepatitis B virus replication through suppression of the interferon signalling pathway.

Persistent chronic infection with hepatitis B virus (HBV) is a major risk factor for the development of HBV- related diseases. The molecular mechanisms that underlie HBV infection and associated carcinogenesis are not fully understood. The aim of this study was to explore the role of ENO1 in HBV replication processes. Here, we examined ENO1 expression levels in HBV- infected and non-HBV- infected liver tissues and cells by Western blot analysis, real- time PCR and immunohistochemistry. In addition, HBsAg and HBeAg in the media of transfected HepG2.2.15 cells were detected using an electrochemical luminescence analyser within 48 hours after ENO1-specific siRNA transfection. The expression levels of HBV DNA, type I interferon and 5 downstream IFN- stimulated genes in HepG2.2.15 cells were examined using real- time PCR. We found ENO1 expression was upregulated in the HBV- infected liver tissues and cells. Silencing of ENO1 resulted in a significant reduction in HBV replication, and this siRNA-mediated reaction also caused the upregulation of expression of type I interferon and downstream IFN- stimulated genes. Therefore, we come to the conclusion ENO1 is involved in HBV replication. It is therefore likely that HBV replication is enhanced following suppression of the IFN signalling pathway. However, the mechanisms that underpin ENO1- mediated modulation of the IFN signalling pathway remain to be elucidated. [ABSTRACT FROM AUTHOR]