Published online Mar 27, 2018. doi: 10.4254/wjh.v10.i3.352
Peer-review started: November 2, 2017
First decision: November 27, 2017
Revised: January 27, 2018
Accepted: February 9, 2018
Article in press: February 9, 2018
Published online: March 27, 2018
Chronic hepatitis B (CHB) is a major global health problem affecting an estimated 350 million people with more than 786000 individuals dying annually due to complications, such as cirrhosis, liver failure and hepatocellular carcinoma (HCC). Liver transplantation (LT) is considered gold standard for treatment of hepatitis B virus (HBV)-related liver failure and HCC. However, post-transplant viral reactivation can be detrimental to allograft function, leading to poor survival. Prophylaxis with high-dose hepatitis B immunoglobulin (HBIG) and anti-viral drugs have achieved remarkable progress in LT by suppressing viral replication and improving long-term survival. The combination of lamivudine (LAM) plus HBIG has been for many years the most widely used. However, life-long HBIG use is both cumbersome and costly, whereas long-term use of LAM results in resistant virus. Recently, in an effort to develop HBIG-free protocols, high potency nucleos(t)ide analogues, such as Entecavir or Tenofovir, have been tried either as monotherapy or in combination with low-dose HBIG with excellent results. Current focus is on novel antiviral targets, especially for covalently closed circular DNA (cccDNA), in an effort to eradicate HBV infection instead of viral suppression. However, there are several other molecular mechanisms through which HBV may reactivate and need equal attention. The purpose of this review is to address post-LT HBV reactivation, its risk factors, underlying molecular mechanisms, and recent advancements and future of anti-viral therapy.
Core tip: Aim of this review is to summarize the current concepts and management of hepatitis B after liver transplantation (LT). There are no clear guidelines regarding hepatitis B therapy after transplantation. Hepatitis B immunoglobulin (HBIG) is expensive and cumbersome to administer and there is no definite time point for discontinuation of HBIG after LT. Here we summarize the indications and duration of hepatitis B immunoglobulin and nucleoside analogs. This review also addresses key molecular mechanisms and the risk factors which are associated with hepatitis B virus reactivation post LT. This review provides up-to-date information not only for the liver transplant specialists but also for the virologists and scientists working in this field.