Heparin sulphate D-glucosaminyl 3-O-sulfotransferase 3B1 plays a role in HBV replication.

Abstract

Hepatitis B virus infection is a worldwide epidemic and is closely associated with the development of hepatocellular carcinoma. Nevertheless, the molecular mechanisms of HBV infection and carcinogenesis remain elusive. Using a hepatocyte model of HBV infection and comparing the gene expression profiling analysis we found that heparan sulfate D-glucosaminyl 3-O-sulfotransferase 3 B1 (HS3ST3B1,3-OST3-B) is down-regulated in the hepatocytes of chronic HBV infection model. HS3ST3B1 showed potent inhibitory effect on HBV replication. The inhibitory effect of HS3ST3B1 overexpression was lost upon gene silencing of HS3ST3B1 or when a catalytic inactive mutant of HS3ST3B1 was expressed. Our study revealed the anti-viral activity of HS3ST3B1 on HBV replication. It is conceivable that possible therapeutic applications of HBV infection could be devised by manipulating HS3ST3B1 activity.

• Authors: Zhenzhen Zhang, Xiang Liu, Juan Chen, Huaibin Su, Qiang Luo, Jia Ye, Ni Tang, Wenlu Zhang, WeiXian Chen, Ben C B Ko, Ailong Huang
• Journal: Virology (Virology) Vol. 406 Issue 2 Pg. 280-5 (Oct 25 2010) ISSN: 1096-0341 [Electronic] United States
• PMID: 20705311 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2010 Elsevier Inc. All rights reserved.

Chemical References

• Sulfotransferases
• heparan sulfate D-glucosaminyl 3-O-sulfotransferase

Topics

• Down-Regulation
• Hep G2 Cells
• Hepatitis B virus (genetics, physiology)
• Hepatitis B, Chronic (enzymology, genetics, virology)
• Hepatocytes (enzymology, virology)
• Humans
• Mutation
• Sulfotransferases (genetics, metabolism)
• Virus Replication