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Viruses 2017, 9(1), 18; doi:10.3390/v9010018

Control of Hepatitis B Virus by Cytokines

1
Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
2
Institute of Virology, Technische Universität München/Helmholtz Zentrum München, Munich 81675, Germany
3
German Center for Infection Research (DZIF), Munich Partner Site, Munich 81675, Germany
*
Author to whom correspondence should be addressed.
Academic Editor: Eric O. Freed
Received: 17 November 2016 / Revised: 13 January 2017 / Accepted: 13 January 2017 / Published: 20 January 2017
(This article belongs to the Special Issue Recent Advances in Hepatitis B Virus Research)
View Full-Text   |   Download PDF [217 KB, uploaded 20 January 2017]

Abstract

Hepatitis B virus (HBV) infection remains a major public health problem worldwide with more than 240 million individuals chronically infected. Current treatments can control HBV replication to a large extent, but cannot eliminate HBV infection. Cytokines have been shown to control HBV replication and contribute to HBV cure in different models. Cytokines play an important role in limiting acute HBV infection in patients and mediate a non-cytolytic clearance of the virus. In this review, we summarize the effects of cytokines and cytokine-induced cellular signaling pathways on different steps of the HBV life cycle, and discuss possible strategies that may contribute to the eradication of HBV through innate immune activation. View Full-Text
Keywords: hepatitis B virus (HBV); cytokine; interferon; interferon-induced gene (ISG); cccDNA; therapy hepatitis B virus (HBV); cytokine; interferon; interferon-induced gene (ISG); cccDNA; therapy
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Xia, Y.; Protzer, U. Control of Hepatitis B Virus by Cytokines. Viruses 2017, 9, 18.

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