Pathological and virological examinations of enterovirus 71 infection: an autopsy case

Gao, Lu; Lin, Pei; Liu, Shu Guang; Chen, Qing; Yu, Shou yi; Shen, Hong

doi:10.1097/01.pat.0000454259.31128.90

Cited by 3 publications

(2 citation statements)

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“…In addition, histopathological analyses revealed focal haemorrhage and accumulation of proteinaceous, erythrocyte-laden transudate in the alveolar spaces. These features closely resembled those observed in non-virally-induced NPE in experimental animal models and human fatal cases 23 29 43 44 45 46 .…”

Section: Discussionsupporting

confidence: 76%

A clinically authentic mouse model of enterovirus 71 (EV-A71)-induced neurogenic pulmonary oedema

Victorio

et al. 2016

Sci Rep

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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.

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Section: Discussionsupporting

confidence: 76%

A clinically authentic mouse model of enterovirus 71 (EV-A71)-induced neurogenic pulmonary oedema

Victorio

et al. 2016

Sci Rep

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“…The neurological disorders result from virus-induced damage and inflammation in various regions of the central nervous system (CNS), including cerebral cortex, brainstem, and spinal cord leading to neurological complications such as aseptic meningitis, brainstem encephalitis, and cardiorespiratory failure (Wang et al, 1999). Pathological examination of fatal EV-A71 cases also revealed viral antigens and RNA in spinal cord and various parts of the brainstem, further reflecting the neurotropism of EV-A71 (Gao et al, 2014;Xing et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Enterovirus‐A71 exploits peripherin and Rac1 to invade the central nervous system

Lim

et al. 2021

EMBO Reports

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Enterovirus-A71 (EV-A71) has been associated with severe neurological forms of hand, foot, and mouth disease (HFMD). EV-A71 infects motor neurons at neuromuscular junctions (NMJs) to invade the central nervous system (CNS). Here, we investigate the role of peripherin (PRPH) during EV-A71 infection, a type III intermediate neurofilament involved in neurodegenerative conditions. In mice infected with EV-A71, PRPH co-localizes with viral particles in the muscles at NMJs and in the spinal cord. In motor neuron-like and neuroblastoma cell lines, surface-expressed PRPH facilitates viral entry, while intracellular PRPH influences viral genome replication through interactions with structural and non-structural viral components. Importantly, PRPH does not play a role during infection with coxsackievirus A16, another causative agent of HFMD rarely associated with neurological complications, suggesting that EV-A71 ability to exploit PRPH represents a unique attribute for successful CNS invasion. Finally, we show that EV-A71 also exploits some of the many PRPH-interacting partners. Of these, small GTP-binding protein Rac1 represents a potential druggable host target to limit neuroinvasion of EV-A71.

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Novel pathological findings and immunohistochemical detection of FMDV antigens in the brain of calves naturally infected with foot-and-mouth disease

Sahoo

Kondabattula

Thakor

et al. 2022

Microbial Pathogenesis

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Pathological and virological examinations of enterovirus 71 infection: an autopsy case

Cited by 3 publications

References 0 publications

A clinically authentic mouse model of enterovirus 71 (EV-A71)-induced neurogenic pulmonary oedema

A clinically authentic mouse model of enterovirus 71 (EV-A71)-induced neurogenic pulmonary oedema

Enterovirus‐A71 exploits peripherin and Rac1 to invade the central nervous system

Novel pathological findings and immunohistochemical detection of FMDV antigens in the brain of calves naturally infected with foot-and-mouth disease

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