Published online May 12, 2015. doi: 10.5501/wjv.v4.i2.36
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
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.