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Research

HBV replication is significantly reduced by IL-6

Tzer-Min Kuo^1,2 , Cheng-po Hu³ , Ya-Ling Chen¹ , Ming-Hsiang Hong^1,2 , King-Song Jeng⁴ , Chun-Chin T Liang⁵ , Mong-Liang Chen^1,6 and Chungming Chang^1,2

¹  Division of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli, Taiwan, ROC

²  Institute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan, ROC

³  Department of life Science, Tunghai University, Taichung, Taiwan, ROC

⁴  Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan, ROC

⁵  Institute of Cellular and System Medicine, National Health Research Institutes, Miaoli, Taiwan, ROC

⁶  Department of General Education, National Taipei College of Nursing, Taipei, Taiwan, ROC

author email corresponding author email

Journal of Biomedical Science 2009, 16:41doi:10.1186/1423-0127-16-41

Published:	20 April 2009

Abstract

Interleukin-6 (IL-6) is a pleiotropic cytokine with pivotal functions in the regulation of the biological responses of several target cells including hepatocytes. The level of serum IL-6 has been reported to be elevated in patients with chronic hepatitis B, cirrhosis and hepatocellular carcinoma and represents the best marker of HBV-related clinical progression as compared with several other cytokines. In this study, we found that IL-6 was able to effectively suppress hepatitis B virus (HBV) replication and prevent the accumulation of HBV covalently closed circular DNA (cccDNA) in a human hepatoma cell line. We also demonstrated that the suppression of HBV replication by IL-6 requires concurrently a moderate reduction of viral transcripts/core proteins and a marked decrease in viral genome-containing nucleocapsids. Studies on the stability of existing viral capsids suggest that the IL-6 effect on the reduction of genome-containing nucleocapsids is mediated through the prevention of the formation of genome-containing nucleocapsids, which is similar to the effect of interferons. However, IFN-α/β and IFN-γ did not participate in the IL-6-induced suppression of HBV replication. Taken together, our results will provide important information to better understand the role of IL-6 in the course of HBV infection.