The metabolic responses to hepatitis B virus infection shed new light on pathogenesis and targets for treatment

Chronic infection caused by the hepatitis B virus (HBV), is strongly associated with hepatitis, fatty liver and hepatocellular carcinoma. To investigate the underlying mechanisms, we characterize the metabolic features of host cells infected with the virus using systems biological approach. The resu...

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Bibliographic Details
Published in:Scientific reports 2015-02, Vol.5 (1), p.8421-8421, Article 8421
Main Authors: Li, Hongde, Zhu, Wandi, Zhang, Leike, Lei, Hehua, Wu, Xiangyu, Guo, Lin, Chen, Xinwen, Wang, Yulan, Tang, Huiru
Format: Article
Language:English
Subjects:
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Biosynthesis
Biosynthetic Pathways
Cell Line, Tumor
Choline
Choline kinase
Chronic infection
Citric Acid Cycle
Extracellular Space
Fatty liver
Fructose
Fructose-6-phosphate
Glutamine
Hepatitis
Hepatitis B
Hepatitis B - drug therapy
Hepatitis B - genetics
Hepatitis B - metabolism
Hepatitis B - virology
Hepatitis B virus - physiology
Hepatitis B, Chronic - drug therapy
Hepatitis B, Chronic - genetics
Hepatitis B, Chronic - metabolism
Hepatitis B, Chronic - virology
Hepatocellular carcinoma
Hexosamines - biosynthesis
Humanities and Social Sciences
Humans
Infections
Intracellular Space
Lecithin
Liver cancer
Magnetic Resonance Spectroscopy
Metabolism
Metabolome
Metabolomics
multidisciplinary
Oxidative Stress
Pathogenesis
Phosphatidylcholine
Phosphatidylcholines - biosynthesis
Replication
Science
Virus Replication
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Summary:Chronic infection caused by the hepatitis B virus (HBV), is strongly associated with hepatitis, fatty liver and hepatocellular carcinoma. To investigate the underlying mechanisms, we characterize the metabolic features of host cells infected with the virus using systems biological approach. The results show that HBV replication induces systematic metabolic alterations in host cells. HBV infection up-regulates the biosynthesis of hexosamine and phosphatidylcholine by activating glutamine-fructose-6-phosphate amidotransferase 1 (GFAT1) and choline kinase alpha (CHKA) respectively, which were reported for the first time for HBV infection. Importantly suppressing hexosamine biosynthesis and phosphatidylcholine biosynthesis can inhibit HBV replication and expression. In addition, HBV induces oxidative stress and stimulates central carbon metabolism and nucleotide synthesis. Our results also indicate that HBV associated hepatocellular carcinoma could be attributed to GFAT1 activated hexosamine biosynthesis and CHKA activated phosphatidylcholine biosynthesis. This study provides further insights into the pathogenesis of HBV-induced diseases and sheds new light on drug target for treating HBV infection.
ISSN:2045-2322
2045-2322
DOI:10.1038/srep08421