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Hepatitis B virus persistence and reactivation
BMJ 2020; 370 doi: https://doi.org/10.1136/bmj.m2200 (Published 01 September 2020) Cite this as: BMJ 2020;370:m2200
Yu Shi, attending physician1 2 3, Min Zheng, professor1 2 3
Author affiliations
1The State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital of School of Medicine, Zhejiang University, Hangzhou, China
2Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China
3National Clinical Research Center for Infectious Diseases, China
Correspondence to M Zheng: [email protected]
Abstract
Hepatitis B virus (HBV) infection causes chronic hepatitis and has long term complications. Individuals ever infected with HBV are at risk of viral reactivation under certain circumstances. This review summarizes studies on HBV persistence and reactivation with a focus on the definitions and mechanisms. Emphasis is placed on the interplay between HBV replication and host immunity as this interplay determines the patterns of persistence following viral acquisition. Chronic infections exhibit as overt persistence when a defective immune response fails to control the viral replication. The HBV genome persists despite an immune response in the form of covalently closed circular DNA (cccDNA) and integrated DNA, rendering an occult state of viral persistence in individuals whose infection appears to have been resolved. We have described HBV reactivation that occurs because of changes in the virus or the immune system. This review aims to raise the awareness of HBV reactivation and to understand how HBV persists, and discusses the risks of HBV reactivation in a variety of clinical settings. |
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发表于 2020-10-5 21:14