ABSTRACT
Recent studies indicate that hepatitis B virus (HBV) can induce autophagy to enhance its replication in cell cultures. To understand whether autophagy can indeed enhance HBV replication in vivo, we generated HBV transgenic mice with liver-specific knockout of the Atg5 gene, a gene critical for the initiation of autophagy. Immunoblot analyses confirmed the inhibition of autophagy in the liver of Atg5-knockout mice. This inhibition of autophagy reduced slightly HBV gene expression and affected nuclear localization of the HBV core protein. It also reduced the HBV DNA level in the sera by more than 90% and the level of HBV DNA replicative intermediate in the mouse liver to an almost undetectable level. Our results thus demonstrate that autophagy is important for HBV replication in vivo and raise the possibility of targeting this pathway to treat HBV patients.
FOOTNOTES
- ↵*To whom correspondence should be addressed. Department of Molecular Microbiology and Immunology, University of Southern California, 2011 Zonal Avenue, HMR-401, Los Angeles, CA 90033; Phone : 323-442-1720 ; FAX : 323-442-1721; E-mail: jamesou{at}hsc.usc.edu
- Copyright © 2011, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
