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

Zhenzhen Zhang; Xiang Liu; Juan Chen; Huaibin Su; Qiang Luo; Jia Ye; Ni Tang; Wenlu Zhang; Wei Xian Chen; Chi Bun Ko; Ailong Huang

doi:10.1016/j.virol.2010.07.030

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

Zhenzhen Zhang, Xiang Liu, Juan Chen, Huaibin Su, Qiang Luo, Jia Ye, Ni Tang, Wenlu Zhang, Wei Xian Chen, Chi Bun Ko, Ailong Huang

Research output: Journal article publication › Journal article › Academic research › peer-review

18 Citations (Scopus)

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.

Original language	English
Pages (from-to)	280-285
Number of pages	6
Journal	Virology
Volume	406
Issue number	2
DOIs	https://doi.org/10.1016/j.virol.2010.07.030
Publication status	Published - 1 Oct 2010
Externally published	Yes

Keywords

Heparan sulfate D-glucosaminyl 3-O-sulfotransferase 3 B1
Hepatitis B virus
Inhibition
Replication

ASJC Scopus subject areas

Virology

More information

10.1016/j.virol.2010.07.030

Cite this

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title = "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.",

keywords = "Heparan sulfate D-glucosaminyl 3-O-sulfotransferase 3 B1, Hepatitis B virus, Inhibition, Replication",

author = "Zhenzhen Zhang and Xiang Liu and Juan Chen and Huaibin Su and Qiang Luo and Jia Ye and Ni Tang and Wenlu Zhang and Chen, {Wei Xian} and Ko, {Chi Bun} and Ailong Huang",

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doi = "10.1016/j.virol.2010.07.030",

language = "English",

volume = "406",

pages = "280--285",

journal = "Virology",

issn = "0042-6822",

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Heparin sulphate d-glucosaminyl 3-O-sulfotransferase 3B1 plays a role in HBV replication. / Zhang, Zhenzhen; Liu, Xiang; Chen, Juan; Su, Huaibin; Luo, Qiang; Ye, Jia; Tang, Ni; Zhang, Wenlu; Chen, Wei Xian; Ko, Chi Bun; Huang, Ailong.

In: Virology, Vol. 406, No. 2, 01.10.2010, p. 280-285.

Research output: Journal article publication › Journal article › Academic research › peer-review

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AU - Liu, Xiang

AU - Chen, Juan

AU - Su, Huaibin

AU - Luo, Qiang

AU - Ye, Jia

AU - Tang, Ni

AU - Zhang, Wenlu

AU - Chen, Wei Xian

AU - Ko, Chi Bun

AU - Huang, Ailong

PY - 2010/10/1

Y1 - 2010/10/1

N2 - 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.

AB - 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.

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KW - Hepatitis B virus

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

Abstract

Keywords

ASJC Scopus subject areas

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