Please use this identifier to cite or link to this item: https://doi.org/10.1128/JVI.00386-17
Title: Serum metabolomics investigation of humanized mouse model of dengue virus infection
Authors: Cui, L
Hou, J
Fang, J 
Lee, Y.H 
Costa, V.V
Wong, L.H
Chen, Q 
Ooi, E.E 
Tannenbaum, S.R
Chen, J
Ong, C.N 
Keywords: acylcarnitine
arachidonic acid
bile acid
linoleic acid
lysine
phenylalanine
phospholipid
purine derivative
pyrimidine derivative
sphingolipid
tryptophan
amino acid synthesis
animal experiment
animal model
arachidonic acid metabolism
Article
bile acid synthesis
biodegradation
dengue
Dengue virus 2
fatty acid oxidation
lipolysis
mass spectrometry
metabolite
metabolome
metabolomics
mouse
mouse model
nonhuman
phospholipid metabolism
priority journal
prognosis
purine metabolism
serum
sphingolipid metabolism
tryptophan metabolism
animal
chemistry
dengue
disease model
metabolome
metabolomics
pathology
SCID mouse
time factor
Animals
Dengue
Disease Models, Animal
Mass Spectrometry
Metabolome
Metabolomics
Mice
Mice, SCID
Serum
Time Factors
Issue Date: 2017
Publisher: American Society for Microbiology
Citation: Cui, L, Hou, J, Fang, J, Lee, Y.H, Costa, V.V, Wong, L.H, Chen, Q, Ooi, E.E, Tannenbaum, S.R, Chen, J, Ong, C.N (2017). Serum metabolomics investigation of humanized mouse model of dengue virus infection. Journal of Virology 91 (14) : e00386-17. ScholarBank@NUS Repository. https://doi.org/10.1128/JVI.00386-17
Abstract: Dengue is an acute febrile illness caused by dengue virus (DENV) and a major cause of morbidity and mortality in tropical and subtropical regions of the world. The lack of an appropriate small-animal model of dengue infection has greatly hindered the study of dengue pathogenesis and the development of therapeutics. In this study, we conducted mass spectrometry-based serum metabolic profiling from a model using humanized mice (humice) with DENV serotype 2 infection at 0, 3, 7, 14, and 28 days postinfection (dpi). Forty-eight differential metabolites were identified, including fatty acids, purines and pyrimidines, acylcarnitines, acylglycines, phospholipids, sphingolipids, amino acids and derivatives, free fatty acids, and bile acid. These metabolites showed a reversible-change trend-most were significantly perturbed at 3 or 7 dpi and returned to control levels at 14 or 28 dpi, indicating that the metabolites might serve as prognostic markers of the disease in humice. The major perturbed metabolic pathways included purine and pyrimidine metabolism, fatty acid ?-oxidation, phospholipid catabolism, arachidonic acid and linoleic acid metabolism, sphingolipid metabolism, tryptophan metabolism, phenylalanine metabolism, lysine biosynthesis and degradation, and bile acid biosynthesis. Most of these disturbed pathways are similar to our previous metabolomics findings in a longitudinal cohort of adult human dengue patients across different infection stages. Our analyses revealed the commonalities of host responses to DENV infection between humice and humans and suggested that humice could be a useful small-animal model for the study of dengue pathogenesis and the development of dengue therapeutics. © 2017 American Society for Microbiology.
Source Title: Journal of Virology
URI: https://scholarbank.nus.edu.sg/handle/10635/175158
ISSN: 0022-538X
DOI: 10.1128/JVI.00386-17
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