Editorial
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Virology. May 12, 2015; 4(2): 36-41
Published online May 12, 2015. doi: 10.5501/wjv.v4.i2.36
Molecular interactions between hepatitis B virus and delta virus
Elham Shirvani-Dastgerdi, Frank Tacke
Elham Shirvani-Dastgerdi, Frank Tacke, Department of Medicine III, University Hospital Aachen, 52074 Aachen, Germany
Author contributions: Shirvani-Dastgerdi E and Tacke F wrote this editorial.
Supported by The German Research Foundation (DFG Ta434/2-1 and SFB/TRR57); and by the Interdisciplinary Center for Clinical Research (IZKF) Aachen.
Conflict-of-interest: The authors declare no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Frank Tacke, MD, PhD, Department of Medicine III, RWTH-University Hospital Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany. frank.tacke@gmx.net
Telephone: +49-241-8035848 Fax: +49-241-8082455
Received: January 13, 2015
Peer-review started: January 15, 2015
First decision: February 7, 2015
Revised: February 12, 2015
Accepted: March 5, 2015
Article in press: March 9, 2015
Published online: May 12, 2015
Processing time: 107 Days and 16.6 Hours
Core Tip

Core tip: Hepatitis D virus (HDV) causes accelerated liver disease in form of fulminant or chronic hepatitis in patients with hepatitis B virus (HBV) infection. HBV supports HDV replication by sharing its surface proteins. Even without overt HBV-DNA replication, transcription of HBV surface proteins (HBsAgs) remains stable in HDV infected cells, which is essential for assembly of HDV virions containing HBsAg proteins. HDV replication is oftentimes associated with a suppression of HBV-DNA levels, and several mechanisms have been suggested how HBV or HDV may influence each other’s replication. Understanding molecular interactions between HBV and HDV may help to design novel therapeutic strategies.