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Article: Phosphatidic acid phosphatase 1 impairs SARS-CoV-2 replication by affecting the glycerophospholipid metabolism pathway

TitlePhosphatidic acid phosphatase 1 impairs SARS-CoV-2 replication by affecting the glycerophospholipid metabolism pathway
Authors
KeywordsCOVID-19
lipidomics
phosphatidic acid phosphatases
SARS-CoV-2
Issue Date2022
Citation
International Journal of Biological Sciences, 2022, v. 18, n. 12, p. 4744-4755 How to Cite?
AbstractViruses exploit the host lipid metabolism machinery to achieve efficient replication. We herein characterize the lipids profile reprogramming in vitro and in vivo using liquid chromatography-mass spectrometry-based untargeted lipidomics. The lipidome of SARS-CoV-2-infected Caco-2 cells was markedly different from that of mock-infected samples, with most of the changes involving downregulation of ceramides. In COVID-19 patients’ plasma samples, a total of 54 lipids belonging to 12 lipid classes that were significantly perturbed compared to non-infected control subjects’ plasma samples were identified. Among these 12 lipid classes, ether-linked phosphatidylcholines, ether-linked phosphatidylethanolamines, phosphatidylcholines, and ceramides were the four most perturbed. Pathway analysis revealed that the glycerophospholipid, sphingolipid, and ether lipid metabolisms pathway were the most significantly perturbed host pathways. Phosphatidic acid phosphatases (PAP) were involved in all three pathways and PAP-1 deficiency significantly suppressed SARS-CoV-2 replication. siRNA knockdown of LPIN2 and LPIN3 resulted in significant reduction of SARS-CoV-2 load. In summary, these findings characterized the host lipidomic changes upon SARS-CoV-2 infection and identified PAP-1 as a potential target for intervention for COVID-19.
Persistent Identifierhttp://hdl.handle.net/10722/315209
ISSN
2023 Impact Factor: 8.2
2023 SCImago Journal Rankings: 2.114
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYan, Bingpeng-
dc.contributor.authorYuan, Shuofeng-
dc.contributor.authorCao, Jianli-
dc.contributor.authorFung, Kingchun-
dc.contributor.authorLai, Pok Man-
dc.contributor.authorYin, Feifei-
dc.contributor.authorSze, Kong Hung-
dc.contributor.authorQin, Zhenzhi-
dc.contributor.authorXie, Yubin-
dc.contributor.authorYe, Zi Wei-
dc.contributor.authorYuen, Terrence Tsz Tai-
dc.contributor.authorChik, Kenn Ka Heng-
dc.contributor.authorTsang, Jessica Oi Ling-
dc.contributor.authorZou, Zijiao-
dc.contributor.authorChan, Chris Chun Yiu-
dc.contributor.authorLuo, Cuiting-
dc.contributor.authorCai, Jian Piao-
dc.contributor.authorChan, Kwok Hung-
dc.contributor.authorChung, Tom Wai Hing-
dc.contributor.authorTam, Anthony Raymond-
dc.contributor.authorChu, Hin-
dc.contributor.authorJin, Dong Yan-
dc.contributor.authorHung, Ivan Fan Ngai-
dc.contributor.authorYuen, Kwok Yung-
dc.contributor.authorKao, Richard Yi Tsun-
dc.contributor.authorChan, Jasper Fuk Woo-
dc.date.accessioned2022-08-05T10:18:03Z-
dc.date.available2022-08-05T10:18:03Z-
dc.date.issued2022-
dc.identifier.citationInternational Journal of Biological Sciences, 2022, v. 18, n. 12, p. 4744-4755-
dc.identifier.issn1449-2288-
dc.identifier.urihttp://hdl.handle.net/10722/315209-
dc.description.abstractViruses exploit the host lipid metabolism machinery to achieve efficient replication. We herein characterize the lipids profile reprogramming in vitro and in vivo using liquid chromatography-mass spectrometry-based untargeted lipidomics. The lipidome of SARS-CoV-2-infected Caco-2 cells was markedly different from that of mock-infected samples, with most of the changes involving downregulation of ceramides. In COVID-19 patients’ plasma samples, a total of 54 lipids belonging to 12 lipid classes that were significantly perturbed compared to non-infected control subjects’ plasma samples were identified. Among these 12 lipid classes, ether-linked phosphatidylcholines, ether-linked phosphatidylethanolamines, phosphatidylcholines, and ceramides were the four most perturbed. Pathway analysis revealed that the glycerophospholipid, sphingolipid, and ether lipid metabolisms pathway were the most significantly perturbed host pathways. Phosphatidic acid phosphatases (PAP) were involved in all three pathways and PAP-1 deficiency significantly suppressed SARS-CoV-2 replication. siRNA knockdown of LPIN2 and LPIN3 resulted in significant reduction of SARS-CoV-2 load. In summary, these findings characterized the host lipidomic changes upon SARS-CoV-2 infection and identified PAP-1 as a potential target for intervention for COVID-19.-
dc.languageeng-
dc.relation.ispartofInternational Journal of Biological Sciences-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectCOVID-19-
dc.subjectlipidomics-
dc.subjectphosphatidic acid phosphatases-
dc.subjectSARS-CoV-2-
dc.titlePhosphatidic acid phosphatase 1 impairs SARS-CoV-2 replication by affecting the glycerophospholipid metabolism pathway-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.7150/ijbs.73057-
dc.identifier.pmid35874954-
dc.identifier.pmcidPMC9305268-
dc.identifier.scopuseid_2-s2.0-85134609734-
dc.identifier.volume18-
dc.identifier.issue12-
dc.identifier.spage4744-
dc.identifier.epage4755-
dc.identifier.isiWOS:000828439300023-

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