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The Effect and Possible Mechanism of Double-Stranded DNA on Replication of Hepatitis B Virus | OMICS International | Abstract
ISSN: 1747-0862

Journal of Molecular and Genetic Medicine
Open Access

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Research Article

The Effect and Possible Mechanism of Double-Stranded DNA on Replication of Hepatitis B Virus

Yan Yang1, Anding Liu1, Shenpei Liu1, Chunyan Zhang1, Xiang Liu1, Hongping Huang1, Jingjiao Song1, Yan Chen1, Yuan Yu1 and Xuefeng Zhou2*

1Experimental Medical Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

2Department of Pediatric Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

Corresponding Author:
Xuefeng Zhou
Department of Pediatric Surgery
Tongji Hospital, Tongji Medical College
Huazhong University of Science and Technology
Wuhan, China
Tel: 13995583508
E-mail: [email protected]

Received Date: September 3, 2013; Accepted Date: November 20, 2013; Published Date: November 25, 2013

Citation: Yang Y, Liu A, Liu S, Zhang C, Liu X, Huang H, et al. (2013) The Effect and Possible Mechanism of Double-Stranded DNA on Replication of Hepatitis B Virus. J Mol Genet Med 7:89. doi:10.4172/1747-0862.1000089

Copyright: © 2013 Yang Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Abstract

Liver is one of the target organs for double-stranded DNA (dsDNA)-vector mediated gene delivery due to the highly efficient uptake of gene therapy vectors. Recently dsDNA was described as a pathogen associated molecular pattern that could be recognized by intracellular DNA sensors. Herein, we explored the possibility that dsDNA may change the intracellular innate immune responses of hepatocyte-derived cell and therefore regulate the replication of hepatitis B virus (HBV). A hepatoma cell line HepG2.2.15 which derived from HepG2 with integrated HBV genome, were treated with poly (dA-dT), a synthetic double-stranded DNA molecule. Unexpectedly, HBV replication was up-regulated after poly (dA-dT) transfection in HepG2.2.15 despite the delayed activation of ISGs. There was no nuclear-plasma translocation of IRF3 or NF-κB observed at a early stage. Treatment of HepG2.2.15 cells with supernatant harvested from the cells transfected with poly (dA-dT) indicating that poly (dA-dT) -enhanced HBV replication was predominantly mediated by not secreted cytokines, but intracellular factors. By blocking the cellular signal pathways with inhibitors, we found that U0126, an inhibitor of ERK1/2, could abolish the poly (dA-dT) enhanced HBV replication. Pathway-scan results also indicated that phosphorylated MEK1/2 was enhanced after poly (dA-dT) transfection. Whether this HBV replicating enhancement is good for HBV infection disease outcome needs to be further investigated.

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