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Diseases 2015, 3(3), 213-220;

HBV Core Protein Enhances Cytokine Production

Department of Gastroenterology and Nephrology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Current Address: Department of General Surgery, First Hospital of Hebei Medical University, Shijiazhuang 050031, China.
Author to whom correspondence should be addressed.
Academic Editor: Stephen L. Chan
Received: 30 July 2015 / Revised: 10 September 2015 / Accepted: 14 September 2015 / Published: 17 September 2015
(This article belongs to the Special Issue Targeted Therapy of Hepatocellular Carcinoma: Present and Future)
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Hepatitis B virus (HBV) infection, a cause of hepatocellular carcinoma (HCC), remains a serious global health concern. HCC development and human hepatocarcinogenesis are associated with hepatic inflammation caused by host interferons and cytokines. This article focused on the association between the HBV core protein, which is one of the HBV-encoding proteins, and cytokine production. The HBV core protein induced the production of interferons and cytokines in human hepatoma cells and in a mouse model. These factors may be responsible for persistent HBV infection and hepatocarcinogenesis. Inhibitors of programmed death (PD)-1 and HBV core and therapeutic vaccines including HBV core might be useful for the treatment of patients with chronic HBV infection. Inhibitors of HBV core, which is important for hepatic inflammation, could be helpful in preventing the progression of liver diseases in HBV-infected patients. View Full-Text
Keywords: HBV; core; cytokine; interferon HBV; core; cytokine; interferon

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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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Kanda, T.; Wu, S.; Sasaki, R.; Nakamura, M.; Haga, Y.; Jiang, X.; Nakamoto, S.; Yokosuka, O. HBV Core Protein Enhances Cytokine Production. Diseases 2015, 3, 213-220.

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