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

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About: Lipidomic Profiling Reveals Significant Perturbations of Intracellular Lipid Homeostasis in Enterovirus-Infected Cells Goto Sponge NotDistinct Permalink

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Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Lipidomic Profiling Reveals Significant Perturbations of Intracellular Lipid Homeostasis in Enterovirus-Infected Cells
Creator	Yuen, Kwok-Yung Chu, Hin Yuan, Shuofeng Yin, Feifei Lai, Pok-Man Sze, Kong-Hung Yan, Bingpeng Chan, Chan, Gabriella Chik, Cyril Fuk-Woo, Jasper Kao, Yi-Tsun Kar-Pui, Susanna Lau, Oi, Jessica Tsang, Ling Yip, Yan Zou, Zijiao
Source	Medline; PMC
abstract	Enterovirus 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.
has issue date	2019-11-26(xsd:dateTime)
bibo:doi	10.3390/ijms20235952
bibo:pmid	31779252
has license	cc-by
sha1sum (hex)	e657fc1a1df1ac7f0e7f45a43d405cfda6cda48d
schema:url	https://doi.org/10.3390/ijms20235952
resource representing a document's title	Lipidomic Profiling Reveals Significant Perturbations of Intracellular Lipid Homeostasis in Enterovirus-Infected Cells
has PubMed Central identifier	PMC6928875
has PubMed identifier	31779252
schema:publication	Int J Mol Sci
resource representing a document's body	covid:e657fc1a1df1ac7f0e7f45a43d405cfda6cda48d#body_text
is schema:about of	named entity 'liquid' named entity 'viral replication' named entity 'incompletely' named entity 'upregulated' named entity 'based' named entity 'suggested' named entity 'INFECTIONS' named entity 'POTENTIAL' named entity 'MASS SPECTROMETRY' named entity 'REVEALED' named entity 'INDUCED' named entity 'SPECIFIC' named entity 'PATHOLOGICAL FEATURES' named entity 'TAKEN' named entity 'HAVE' named entity 'INFECTION' named entity 'CHARACTERIZED' named entity 'OUR' named entity 'COXSACKIEVIRUS A16' named entity 'STATE' named entity 'CELL CULTURES' named entity 'ADDITION' named entity 'CHANGE IN' named entity 'EXOGENOUS' named entity 'STAGES' named entity 'EFFICIENT' named entity 'MOUTH DISEASE' named entity 'UNDERSTOOD' named entity 'VIRUS INFECTION' named entity 'LIPID' named entity 'INCLUDING' named entity 'LIPIDOMICS' named entity 'PLAY' named entity 'FOOT' named entity 'EPA' named entity 'COMPLICATIONS' named entity 'DISRUPTED' named entity 'PATHWAYS' named entity 'VIRUS REPLICATION CYCLE' named entity 'BASED' named entity 'LIPID CLASSES' named entity 'END' named entity 'ARACHIDONIC ACID' named entity 'TIME OF FLIGHT' named entity 'MECHANISMS' named entity 'HIGH PERFORMANCE LIQUID CHROMATOGRAPHY' named entity 'A71' named entity 'PATHOGENIC' named entity 'RESULTS' named entity 'LIPIDS' named entity 'COMMON' named entity 'POLYUNSATURATED FATTY ACIDS' named entity 'TO CHARACTERIZE' named entity 'ROLES' named entity 'VIRAL REPLICATION' named entity 'LIPIDOME' named entity 'SUPPLYING' named entity 'HAND' named entity 'DOCOSAHEXAENOIC ACID' named entity 'PERFORMED' named entity 'STRATEGY' named entity 'CRITICAL' named entity 'DHA' named entity 'FAX'

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