Published online Jan 7, 2016. doi: 10.3748/wjg.v22.i1.145
Peer-review started: June 3, 2015
First decision: July 14, 2015
Revised: August 19, 2015
Accepted: December 1, 2015
Article in press: December 1, 2015
Published online: January 7, 2016
Core tip: Hepatitis B virus (HBV) is a global health problem, with almost 2 billion infected persons, many of whom deemed to develop chronic carrier state and eventually die from cirrhosis or liver cancer. Unlike in other DNA viruses, its high mutation rate and replicative capability arise considerable genetic variability, recently analyzed by molecular biology tools. HBV mutations occur in all four overlapping open reading frames encoding viral polymerase, surface antigen, core and X protein. Understanding the correlation between mutations and liver disease progression is crucial for an effective clinical management in HBV patients with resistance to antiviral drugs, hepatitis B surface antigen escape mutant, “occult” hepatitis and hepatocellular carcinoma.