Stimulated phospholipid synthesis is key for hepatitis B virus replications
Chronic hepatitis B Virus (HBV) infection has high morbidity, high pathogenicity and unclear pathogenesis. To elucidate the relationship between HBV replication and host phospholipid metabolites, we measured 10 classes of phospholipids in serum of HBV infected patients and cells using ultra performa...
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sg-ntu-dr.10356-1423412020-11-01T05:13:39Z Stimulated phospholipid synthesis is key for hepatitis B virus replications Huang, Qingxia Lei, Hehua Ding, Laifeng Wang, Yulan Lee Kong Chian School of Medicine (LKCMedicine) Singapore Phenome Center Science::Medicine Hepatitis B Virus (HBV) Phospholipid Chronic hepatitis B Virus (HBV) infection has high morbidity, high pathogenicity and unclear pathogenesis. To elucidate the relationship between HBV replication and host phospholipid metabolites, we measured 10 classes of phospholipids in serum of HBV infected patients and cells using ultra performance liquid chromatograph-triple quadruple mass spectrometry. We found that the levels of phosphatidylcholine (PC), phosphatidylethanolamine, and lyso-phosphatidic acid were increased in HBsAg (+) serum of infected patients compared with HBsAg (-), while phosphatidylserine, phosphatidylglycerol, phosphatidylinositol, and sphingomyelin were decreased, which were confirmed in an HBV infected HepG2.2.15 cell line. We further evaluated the enzyme levels of PC pathways and found that PCYT1A and LPP1 for PC synthesis were up-regulated after HBV infection. Moreover, HBV replication was inhibited when PCYT1A and LPP1 were inhibited. These results indicated that the PC synthesis in HBV infected host are regulated by PCYT1A and LPP1, which suggests that PCYT1A, LPP1 could be new potential targets for HBV treatment. Published version 2020-06-19T05:14:30Z 2020-06-19T05:14:30Z 2019 Journal Article Huang, Q., Lei, H., Ding, L., & Wang, Y. (2019). Stimulated phospholipid synthesis is key for hepatitis B virus replications. Scientific Reports, 9(1), 12989-. doi:10.1038/s41598-019-49367-8 2045-2322 https://hdl.handle.net/10356/142341 10.1038/s41598-019-49367-8 31506451 2-s2.0-85072046890 1 9 en Scientific Reports © 2019 The Author(s). This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Te images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. application/pdf |
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Science::Medicine Hepatitis B Virus (HBV) Phospholipid Huang, Qingxia Lei, Hehua Ding, Laifeng Wang, Yulan Stimulated phospholipid synthesis is key for hepatitis B virus replications |
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Chronic hepatitis B Virus (HBV) infection has high morbidity, high pathogenicity and unclear pathogenesis. To elucidate the relationship between HBV replication and host phospholipid metabolites, we measured 10 classes of phospholipids in serum of HBV infected patients and cells using ultra performance liquid chromatograph-triple quadruple mass spectrometry. We found that the levels of phosphatidylcholine (PC), phosphatidylethanolamine, and lyso-phosphatidic acid were increased in HBsAg (+) serum of infected patients compared with HBsAg (-), while phosphatidylserine, phosphatidylglycerol, phosphatidylinositol, and sphingomyelin were decreased, which were confirmed in an HBV infected HepG2.2.15 cell line. We further evaluated the enzyme levels of PC pathways and found that PCYT1A and LPP1 for PC synthesis were up-regulated after HBV infection. Moreover, HBV replication was inhibited when PCYT1A and LPP1 were inhibited. These results indicated that the PC synthesis in HBV infected host are regulated by PCYT1A and LPP1, which suggests that PCYT1A, LPP1 could be new potential targets for HBV treatment. |
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Lee Kong Chian School of Medicine (LKCMedicine) |
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Lee Kong Chian School of Medicine (LKCMedicine) Huang, Qingxia Lei, Hehua Ding, Laifeng Wang, Yulan |
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Article |
author |
Huang, Qingxia Lei, Hehua Ding, Laifeng Wang, Yulan |
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Huang, Qingxia |
title |
Stimulated phospholipid synthesis is key for hepatitis B virus replications |
title_short |
Stimulated phospholipid synthesis is key for hepatitis B virus replications |
title_full |
Stimulated phospholipid synthesis is key for hepatitis B virus replications |
title_fullStr |
Stimulated phospholipid synthesis is key for hepatitis B virus replications |
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Stimulated phospholipid synthesis is key for hepatitis B virus replications |
title_sort |
stimulated phospholipid synthesis is key for hepatitis b virus replications |
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2020 |
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https://hdl.handle.net/10356/142341 |
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1683493232966631424 |