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Reactivation of hepatitis B after liver transplantation: Current knowledge, molecular mechanisms and implications in management

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World Journal of Hepatology 2018年第3期10卷 352-370页

作者： Ranjit Chauhan Shilpa Lingala Chiranjeevi Gadiparthi nivedita lahiri Smruti R Mohanty Jian Wu Tomasz I Michalak Sanjaya K Satapathy Molecular Virology and Hepatology Research Group Division of Bio Medical SciencesHealth Sciences Centre Memorial University Division of Transplant Surgery Methodist University Hospital Transplant Institute University of Tennessee Health Sciences Center Division of Rheumatology Immunology and Allergy Brigham Women's Hospital Harvard Medical School Division of Gastroenterology and Hepatobiliary Disease New York-Presbyterian Brooklyn Methodist Hospital Department of Medical Microbiology Key Laboratory of Molecular Virology Fudan University School of Basic Medical Sciences

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 suppressingviral 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(ccc DNA), 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.

关键词： Hepatitis B virus Liver transplantation Reactivation Hepatitis B immunoglobulin Recurrence Prophylaxis Antivirals

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