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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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Autores principales: Huang, Qingxia, Lei, Hehua, Ding, Laifeng, Wang, Yulan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6736851/
https://www.ncbi.nlm.nih.gov/pubmed/31506451
http://dx.doi.org/10.1038/s41598-019-49367-8
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author Huang, Qingxia
Lei, Hehua
Ding, Laifeng
Wang, Yulan
author_facet Huang, Qingxia
Lei, Hehua
Ding, Laifeng
Wang, Yulan
author_sort Huang, Qingxia
collection PubMed
description 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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spelling pubmed-67368512019-09-20 Stimulated phospholipid synthesis is key for hepatitis B virus replications Huang, Qingxia Lei, Hehua Ding, Laifeng Wang, Yulan Sci Rep Article 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. Nature Publishing Group UK 2019-09-10 /pmc/articles/PMC6736851/ /pubmed/31506451 http://dx.doi.org/10.1038/s41598-019-49367-8 Text en © The Author(s) 2019 Open Access 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. The 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/.
spellingShingle Article
Huang, Qingxia
Lei, Hehua
Ding, Laifeng
Wang, Yulan
Stimulated phospholipid synthesis is key for hepatitis B virus replications
title 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
title_full_unstemmed Stimulated phospholipid synthesis is key for hepatitis B virus replications
title_short Stimulated phospholipid synthesis is key for hepatitis B virus replications
title_sort stimulated phospholipid synthesis is key for hepatitis b virus replications
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6736851/
https://www.ncbi.nlm.nih.gov/pubmed/31506451
http://dx.doi.org/10.1038/s41598-019-49367-8
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