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Article: Lipidomic Profiling Reveals Significant Perturbations of Intracellular Lipid Homeostasis in Enterovirus-Infected Cells

TitleLipidomic Profiling Reveals Significant Perturbations of Intracellular Lipid Homeostasis in Enterovirus-Infected Cells
Authors
Keywordsenterovirus
fatty acid
lipidomics
UPLC-ESI-Q-TOF-MS
Issue Date2019
PublisherMolecular Diversity Preservation International. The Journal's web site is located at http://www.mdpi.org/ijms
Citation
International Journal of Molecular Sciences, 2019, v. 20, p. article no. 5952 How to Cite?
AbstractEnterovirus A71 (EV-A71) and coxsackievirus A16 (CV-A16) are the most common causes of hand, foot, and mouth disease. Severe EV-A71 and CV-A16 infections may be associated with life-threatening complications. However, the pathogenic mechanisms underlying these severe clinical and pathological features remain incompletely understood. Lipids are known to play critical roles in multiple stages of the virus replication cycle. The specific lipid profile induced upon virus infection is required for optimal virus replication. The perturbations in the host cell lipidomic profiles upon enterovirus infection have not been fully characterized. To this end, we performed ultra-high performance liquid chromatography–electrospray ionization–quadrupole–time of flight-mass spectrometry (UPLC-ESI-Q-TOF-MS)-based lipidomics to characterize the change in host lipidome upon EV-A71 and CV-A16 infections. Our results revealed that 47 lipids within 11 lipid classes were significantly perturbed after EV-A71 and CV-A16 infection. Four polyunsaturated fatty acids (PUFAs), namely, arachidonic acid (AA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and eicosapentaenoic acid (EPA), were consistently upregulated upon EV-A71 and CV-A16 infection. Importantly, exogenously supplying three of these four PUFAs, including AA, DHA, and EPA, in cell cultures significantly reduced EV-A71 and CV-A16 replication. Taken together, our results suggested that enteroviruses might specifically modulate the host lipid pathways for optimal virus replication. Excessive exogenous addition of lipids that disrupted this delicate homeostatic state could prevent efficient viral replication. Precise manipulation of the host lipid profile might be a potential host-targeting antiviral strategy for enterovirus infection.
Persistent Identifierhttp://hdl.handle.net/10722/281892
ISSN
2011 Impact Factor: 2.598
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorYan, B-
dc.contributor.authorZou, Z-
dc.contributor.authorChu, H-
dc.contributor.authorChan, G-
dc.contributor.authorTsang, JO-L-
dc.contributor.authorLai, P-M-
dc.contributor.authorYuan, S-
dc.contributor.authorYip, CC-Y-
dc.contributor.authorYin, F-
dc.contributor.authorKao, RY-T-
dc.contributor.authorSze, K-H-
dc.contributor.authorLau, SK-P-
dc.contributor.authorChan, JF-W-
dc.contributor.authorYuen, K-Y-
dc.date.accessioned2020-04-03T07:23:15Z-
dc.date.available2020-04-03T07:23:15Z-
dc.date.issued2019-
dc.identifier.citationInternational Journal of Molecular Sciences, 2019, v. 20, p. article no. 5952-
dc.identifier.issn1661-6596-
dc.identifier.urihttp://hdl.handle.net/10722/281892-
dc.description.abstractEnterovirus A71 (EV-A71) and coxsackievirus A16 (CV-A16) are the most common causes of hand, foot, and mouth disease. Severe EV-A71 and CV-A16 infections may be associated with life-threatening complications. However, the pathogenic mechanisms underlying these severe clinical and pathological features remain incompletely understood. Lipids are known to play critical roles in multiple stages of the virus replication cycle. The specific lipid profile induced upon virus infection is required for optimal virus replication. The perturbations in the host cell lipidomic profiles upon enterovirus infection have not been fully characterized. To this end, we performed ultra-high performance liquid chromatography–electrospray ionization–quadrupole–time of flight-mass spectrometry (UPLC-ESI-Q-TOF-MS)-based lipidomics to characterize the change in host lipidome upon EV-A71 and CV-A16 infections. Our results revealed that 47 lipids within 11 lipid classes were significantly perturbed after EV-A71 and CV-A16 infection. Four polyunsaturated fatty acids (PUFAs), namely, arachidonic acid (AA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and eicosapentaenoic acid (EPA), were consistently upregulated upon EV-A71 and CV-A16 infection. Importantly, exogenously supplying three of these four PUFAs, including AA, DHA, and EPA, in cell cultures significantly reduced EV-A71 and CV-A16 replication. Taken together, our results suggested that enteroviruses might specifically modulate the host lipid pathways for optimal virus replication. Excessive exogenous addition of lipids that disrupted this delicate homeostatic state could prevent efficient viral replication. Precise manipulation of the host lipid profile might be a potential host-targeting antiviral strategy for enterovirus infection.-
dc.languageeng-
dc.publisherMolecular Diversity Preservation International. The Journal's web site is located at http://www.mdpi.org/ijms-
dc.relation.ispartofInternational Journal of Molecular Sciences-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectenterovirus-
dc.subjectfatty acid-
dc.subjectlipidomics-
dc.subjectUPLC-ESI-Q-TOF-MS-
dc.titleLipidomic Profiling Reveals Significant Perturbations of Intracellular Lipid Homeostasis in Enterovirus-Infected Cells-
dc.typeArticle-
dc.identifier.emailYan, B: ybp1205@hku.hk-
dc.identifier.emailChu, H: hinchu@hku.hk-
dc.identifier.emailChan, G: gchan2@hku.hk-
dc.identifier.emailLai, P-M: vangor@hku.hk-
dc.identifier.emailYuan, S: yuansf@hku.hk-
dc.identifier.emailYip, CC-Y: yipcyril@hku.hk-
dc.identifier.emailKao, RY-T: rytkao@hkucc.hku.hk-
dc.identifier.emailSze, K-H: khsze@hku.hk-
dc.identifier.emailLau, SK-P: skplau@hkucc.hku.hk-
dc.identifier.emailChan, JF-W: jfwchan@hku.hk-
dc.identifier.emailYuen, K-Y: kyyuen@hkucc.hku.hk-
dc.identifier.authorityChu, H=rp02125-
dc.identifier.authorityYuan, S=rp02640-
dc.identifier.authorityYip, CC-Y=rp01721-
dc.identifier.authorityKao, RY-T=rp00481-
dc.identifier.authoritySze, K-H=rp00785-
dc.identifier.authorityLau, SK-P=rp00486-
dc.identifier.authorityChan, JF-W=rp01736-
dc.identifier.authorityYuen, K-Y=rp00366-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3390/ijms20235952-
dc.identifier.pmid31779252-
dc.identifier.pmcidPMC6928875-
dc.identifier.scopuseid_2-s2.0-85075495960-
dc.identifier.hkuros309650-
dc.identifier.volume20-
dc.identifier.spagearticle no. 5952-
dc.identifier.epagearticle no. 5952-
dc.publisher.placeSwitzerland-

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