A clinically authentic mouse model of enterovirus 71 (EV-A71)-induced neurogenic pulmonary oedema
| Autor: | Beng Hooi Chua, Kaw Bing Chua, Carla Bianca Luena Victorio, Yishi Xu, Qimei Ng, Sylvie Alonso, Vincent T. K. Chow |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Pathology medicine.medical_specialty Viral pathogenesis Pulmonary Edema Kaplan-Meier Estimate Disease Severity of Illness Index Article Mice 03 medical and health sciences Catecholamines 0302 clinical medicine Enterovirus Infections Enterovirus 71 Animals Humans Medicine Lung Neurotropic virus Mice Inbred BALB C Multidisciplinary Respiratory distress biology business.industry Brain Pulmonary edema medicine.disease biology.organism_classification Antibodies Neutralizing Enterovirus A Human Disease Models Animal 030104 developmental biology medicine.anatomical_structure Immunology Histopathology business 030217 neurology & neurosurgery |
| Zdroj: | Scientific Reports |
| ISSN: | 2045-2322 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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