Please use this identifier to cite or link to this item: https://doi.org/10.1038/srep28876
Title: A clinically authentic mouse model of enterovirus 71 (EV-A71)-induced neurogenic pulmonary oedema
Authors: Victorio, C.B.L 
Xu, Y
Ng, Q
Chua, B.H
Alonso, S 
Chow, V.T.K 
Chua, K.B
Keywords: catecholamine
neutralizing antibody
animal
Bagg albino mouse
blood
brain
disease model
Enterovirus A
Enterovirus infection
human
immunology
Kaplan Meier method
lung
lung edema
metabolism
mortality
mouse
pathology
physiology
severity of illness index
virology
Animals
Antibodies, Neutralizing
Brain
Catecholamines
Disease Models, Animal
Enterovirus A, Human
Enterovirus Infections
Humans
Kaplan-Meier Estimate
Lung
Mice
Mice, Inbred BALB C
Pulmonary Edema
Severity of Illness Index
Issue Date: 2016
Publisher: Nature Publishing Group
Citation: Victorio, C.B.L, Xu, Y, Ng, Q, Chua, B.H, Alonso, S, Chow, V.T.K, Chua, K.B (2016). A clinically authentic mouse model of enterovirus 71 (EV-A71)-induced neurogenic pulmonary oedema. Scientific Reports 6 : 28876. ScholarBank@NUS Repository. https://doi.org/10.1038/srep28876
Abstract: Enterovirus 71 (EV-A71) is a neurotropic virus that sporadically causes fatal neurologic illness among infected children. Animal models of EV-A71 infection exist, but they do not recapitulate in animals the spectrum of disease and pathology observed in fatal human cases. Specifically, neurogenic pulmonary oedema (NPE) - the main cause of EV-A71 infection-related mortality - is not observed in any of these models. This limits their utility in understanding viral pathogenesis of neurologic infections. We report the development of a mouse model of EV-A71 infection displaying NPE in severely affected animals. We inoculated one-week-old BALB/c mice with an adapted EV-A71 strain and identified clinical signs consistent with observations in human cases and other animal models. We also observed respiratory distress in some mice. At necropsy, we found their lungs to be heavier and incompletely collapsed compared to other mice. Serum levels of catecholamines and histopathology of lung and brain tissues of these mice strongly indicated onset of NPE. The localization of virally-induced brain lesions also suggested a potential pathogenic mechanism for EV-A71-induced NPE. This novel mouse model of virally-induced NPE represents a valuable resource for studying viral mechanisms of neuro-pathogenesis and pre-clinical testing of potential therapeutics and prophylactics against EV-A71-related neurologic complications.
Source Title: Scientific Reports
URI: https://scholarbank.nus.edu.sg/handle/10635/174951
ISSN: 20452322
DOI: 10.1038/srep28876
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