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World J Hepatol. May 18, 2015; 7(8): 1097-1104
Published online May 18, 2015. doi: 10.4254/wjh.v7.i8.1097
Role of antiviral therapy in the natural history of hepatitis B virus-related chronic liver disease
Francesco Paolo Russo, Kryssia Rodríguez-Castro, Laura Scribano, Giorgia Gottardo, Veronica Vanin, Fabio Farinati
Francesco Paolo Russo, Kryssia Rodríguez-Castro, Gastroenterology/Multiviseral Transplant Unit, Department of Surgery, Oncology and Gastroenterology, Padua University Hospital, 35128 PD Padua, Italy
Laura Scribano, Giorgia Gottardo, Veronica Vanin, Fabio Farinati, Gastroenterology Unit, Department of Surgery, Oncology and Gastroenterology, Padua University Hospital, 35128 PD Padua, Italy
Author contributions: Russo FP wrote and edited the paper; Scribano L, Gottardo G and Vanin V performed PubMed research and contributed to the discussion; Rodríguez-Castro K performed the revision of the manuscript and contributed to manuscript preparation; Farinati F shared the concepts with Russo FP and edited the paper.
Conflict-of-interest: All of the authors declare they have no conflicts 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: Francesco Paolo Russo, MD, PhD, Gastroenterology/Multiviseral Transplant Unit, Department of Surgery, Oncology and Gastroenterology, Padua University Hospital, Via Giustiniani 2, 35128 PD Padua, Italy. francescopaolo.russo@unipd.it
Telephone: +39-049-8217024 Fax: +39-049-8760820
Received: September 12, 2014
Peer-review started: September 13, 2014
First decision: September 28, 2014
Revised: January 22, 2015
Accepted: February 9, 2015
Article in press: February 11, 2015
Published online: May 18, 2015
Processing time: 249 Days and 15.1 Hours
Abstract

Hepatitis B virus (HBV) infection is a dynamic state of interactions among HBV, hepatocytes, and the host immune system. Natural history studies of chronic hepatitis B (CHB) infection have shown an association between active viral replication and adverse clinical outcomes such as cirrhosis and hepatocellular carcinoma. The goal of therapy for CHB is to improve quality of life and survival by preventing progression of the disease to cirrhosis, decompensation, end-stage liver disease, hepatocellular carcinoma (HCC) and death. This goal can be achieved if HBV replication is suppressed in a sustained manner. The accompanying reduction in histological activity of CHB lessens the risk of cirrhosis and of HCC, particularly in non-cirrhotic patients. However, CHB infection cannot be completely eradicated, due to the persistence of covalently closed circular DNA in the nucleus of infected hepatocytes, which may explain HBV reactivation. Moreover, the integration of the HBV genome into the host genome may favour oncogenesis, development of HCC and may also contribute to HBV reactivation.

Keywords: Hepatocellular carcinoma; Nucleos(t)ide analogues; Liver fibrosis; Pegylated interferon; Cirrhosis

Core tip: The goal of therapy for chronic hepatitis B is to improve quality of life and survival by preventing progression of the disease to cirrhosis, decompensation, end-stage liver disease, hepatocellular carcinoma and death. Current therapeutic options do not eradicate hepatitis B virus (HBV) infection, since HBV remains either integrated in the host genome or in the nuclei of hepatocytes as covalently closed circular DNA, a fact that may favour oncogenesis towards the development of hepatocellular carcinoma, and explains HBV reactivation. It is mandatory for clinicians to start viral suppression in patients with active chronic liver disease, particularly in patients who have already developed advanced hepatic disease.