Epiregulin as a key molecule to suppress hepatitis B virus propagation in vitro

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1: Arch Virol. 2008 Nov 26. [Epub ahead of print]

Epiregulin as a key molecule to suppress hepatitis B virus propagation in vitro.

Ding X, Wang F, Duan M, Yang J, Wang S.

Beijing Institute of Radiation Medicine, 27 Taiping Road, Haidian District,

Beijing, 100850, People's Republic of China.

Hepatitis B virus (HBV) infection is a major health concern around the world,

and only a minority of patients receiving current treatments achieve a sustained

response following a short course of therapy. The majority of patients require

prolonged therapy to suppress viral replication. However, several recent reports

show that inhibiting host-cell proteins can prevent viral infection. Human

epiregulin (EREG) was confirmed by our previous study to be up-regulated in

HepG2.2.15 cells while down-regulated by lamivudine. Therefore, the question was

asked whether inhibiting EREG could prevent viral infection. To address this

question, antisense oligonucleiotides (ASODNs) were used to down-regulate EREG

expression in HepG2.2.15 cells. We were able to show that HBV propagation in

HepG2.2.15 cell culture was reduced in a dose-dependent manner by EREG

inhibition. In addition, we found that treatment with ASODNs did not affect

HepG2.2.15 cell viability. To probe the role of EREG in HBV replication, the

interaction between EREG and HBsAg was also verified using

co-immunoprecipitation and GST pull-down assays. We observed that EREG can

contribute to HBsAg binding to HepG2 cells. In summary, this study demonstrates

that EREG is essential for HBV replication and also provides some evidence for

the potential role of EREG in HBsAg binding.

PMID: 19034604 [PubMed - as supplied by publisher]