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Article: Characterization of the Lipidomic Profile of Human Coronavirus-Infected Cells: Implications for Lipid Metabolism Remodeling upon Coronavirus Replication

TitleCharacterization of the Lipidomic Profile of Human Coronavirus-Infected Cells: Implications for Lipid Metabolism Remodeling upon Coronavirus Replication
Authors
KeywordsHCoV-229E
Lipidomics
MERS-CoV
MS
UHPLC
Issue Date2019
PublisherMolecular Diversity Preservation International (MDPI) AG.. The Journal's web site is located at http://www.mdpi.com/journal/viruses
Citation
Viruses, 2019, v. 11 n. 1, article no. 73 How to Cite?
AbstractLipids play numerous indispensable cellular functions and are involved in multiple steps in the replication cycle of viruses. Infections by human-pathogenic coronaviruses result in diverse clinical outcomes, ranging from self-limiting flu-like symptoms to severe pneumonia with extrapulmonary manifestations. Understanding how cellular lipids may modulate the pathogenicity of human-pathogenic coronaviruses remains poor. To this end, we utilized the human coronavirus 229E (HCoV-229E) as a model coronavirus to comprehensively characterize the host cell lipid response upon coronavirus infection with an ultra-high performance liquid chromatography-mass spectrometry (UPLC–MS)-based lipidomics approach. Our results revealed that glycerophospholipids and fatty acids (FAs) were significantly elevated in the HCoV-229E-infected cells and the linoleic acid (LA) to arachidonic acid (AA) metabolism axis was markedly perturbed upon HCoV-229E infection. Interestingly, exogenous supplement of LA or AA in HCoV-229E-infected cells significantly suppressed HCoV-229E virus replication. Importantly, the inhibitory effect of LA and AA on virus replication was also conserved for the highly pathogenic Middle East respiratory syndrome coronavirus (MERS-CoV). Taken together, our study demonstrated that host lipid metabolic remodeling was significantly associated with human-pathogenic coronavirus propagation. Our data further suggested that lipid metabolism regulation would be a common and druggable target for coronavirus infections. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
Persistent Identifierhttp://hdl.handle.net/10722/273965
ISSN
2017 Impact Factor: 3.761
2015 SCImago Journal Rankings: 1.873
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYan, B-
dc.contributor.authorChu, H-
dc.contributor.authorYang, D-
dc.contributor.authorSze, KH-
dc.contributor.authorLai, PM-
dc.contributor.authorYuan, S-
dc.contributor.authorShuai, HV-
dc.contributor.authorWang, Y-
dc.contributor.authorKao, RYT-
dc.contributor.authorChan, JFW-
dc.contributor.authorYuen, KY-
dc.date.accessioned2019-08-18T14:52:18Z-
dc.date.available2019-08-18T14:52:18Z-
dc.date.issued2019-
dc.identifier.citationViruses, 2019, v. 11 n. 1, article no. 73-
dc.identifier.issn1999-4915-
dc.identifier.urihttp://hdl.handle.net/10722/273965-
dc.description.abstractLipids play numerous indispensable cellular functions and are involved in multiple steps in the replication cycle of viruses. Infections by human-pathogenic coronaviruses result in diverse clinical outcomes, ranging from self-limiting flu-like symptoms to severe pneumonia with extrapulmonary manifestations. Understanding how cellular lipids may modulate the pathogenicity of human-pathogenic coronaviruses remains poor. To this end, we utilized the human coronavirus 229E (HCoV-229E) as a model coronavirus to comprehensively characterize the host cell lipid response upon coronavirus infection with an ultra-high performance liquid chromatography-mass spectrometry (UPLC–MS)-based lipidomics approach. Our results revealed that glycerophospholipids and fatty acids (FAs) were significantly elevated in the HCoV-229E-infected cells and the linoleic acid (LA) to arachidonic acid (AA) metabolism axis was markedly perturbed upon HCoV-229E infection. Interestingly, exogenous supplement of LA or AA in HCoV-229E-infected cells significantly suppressed HCoV-229E virus replication. Importantly, the inhibitory effect of LA and AA on virus replication was also conserved for the highly pathogenic Middle East respiratory syndrome coronavirus (MERS-CoV). Taken together, our study demonstrated that host lipid metabolic remodeling was significantly associated with human-pathogenic coronavirus propagation. Our data further suggested that lipid metabolism regulation would be a common and druggable target for coronavirus infections. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.-
dc.languageeng-
dc.publisherMolecular Diversity Preservation International (MDPI) AG.. The Journal's web site is located at http://www.mdpi.com/journal/viruses-
dc.relation.ispartofViruses-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectHCoV-229E-
dc.subjectLipidomics-
dc.subjectMERS-CoV-
dc.subjectMS-
dc.subjectUHPLC-
dc.titleCharacterization of the Lipidomic Profile of Human Coronavirus-Infected Cells: Implications for Lipid Metabolism Remodeling upon Coronavirus Replication-
dc.typeArticle-
dc.identifier.emailYan, B: ybp1205@hku.hk-
dc.identifier.emailChu, H: hinchu@hku.hk-
dc.identifier.emailSze, KH: khsze@hku.hk-
dc.identifier.emailLai, PM: vangor@hku.hk-
dc.identifier.emailYuan, S: yuansf@hku.hk-
dc.identifier.emailShuai, HV: shuaihp@connect.hku.hk-
dc.identifier.emailKao, RYT: rytkao@hkucc.hku.hk-
dc.identifier.emailChan, JFW: jfwchan@hku.hk-
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hk-
dc.identifier.authorityChu, H=rp02125-
dc.identifier.authoritySze, KH=rp00785-
dc.identifier.authorityKao, RYT=rp00481-
dc.identifier.authorityChan, JFW=rp01736-
dc.identifier.authorityYuen, KY=rp00366-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3390/v11010073-
dc.identifier.pmid30654597-
dc.identifier.scopuseid_2-s2.0-85060147134-
dc.identifier.hkuros301140-
dc.identifier.volume11-
dc.identifier.issue1-
dc.identifier.spagearticle no. 73-
dc.identifier.epagearticle no. 73-
dc.identifier.isiWOS:000459132000072-
dc.publisher.placeSwitzerland-

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