Why the study?
Echovirus 30 causes a wide spectrum of diseases, notably aseptic meningitis outbreaks, motivating the establishment of an animal model to observe induced pathological changes.
This study establishes a novel neonatal mouse model for Echovirus 30 infection, demonstrating its neurotropism and associated pathological and transcriptomic changes.
Hypothesis-generating for E30 neurotropism; extends animal models but leaves open human translation and therapeutic implications.
Echovirus 30 (E30) infection causes a wide spectrum of diseases with mild symptoms, such as hand, foot, and mouth disease (HFMD), acute flaccid paralysis, and aseptic meningitis and other diseases, especially one of the most common pathogens causing aseptic meningitis outbreaks. We established a novel mouse model of E30 infection by inoculating neonatal mice with clinical isolates of E30 and observed the pathological changes induced by E30. Using the E30 infection model, we found complement responses and neuropathy-related genes in the mice tissues at the transcriptome level. Moreover, we found that the viral dsRNA localized in the mouse brain and could replicate in human glioma cell line U251 rather than in the neuroblastoma cell line, SK-N-SH.
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Li et al. (2022) studied this question.
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