Abstract

BackgroundCoxsackievirus commonly infects children and occasionally causes severe meningitis and/or encephalitis in the newborn. The underlying mechanism(s) behind the central nervous system pathology is poorly defined.MethodsIt is hypothesized that astrocytes may be involved in inflammatory response induced by CVB3 infection. Here we discuss this hypothesis in the context of CVB3 infection and associated inflammatory response in primary mouse astrocytes.ResultsThe results showed that coxsackievirus receptor (CAR) was distributed homogeneously on the astrocytes, and that CVB3 could infect and replicate in astrocytes, with release of infectious virus particles. CVB3 induced cytopathic effect and production of proinflammatory cytokines IL-1β, TNF-α, IL-6, and chemokine CXCL10 from astrocytes.ConclusionThese data suggest that direct astrocyte damage and cytokines induction could be a mechanism of virus-induced meningitis and/or encephalitis.

Highlights

  • Coxsackievirus commonly infects children and occasionally causes severe meningitis and/or encephalitis in the newborn

  • Our preliminary study showed that microglia were spared from Coxsackievirus B3 (CVB3) infection, whereas the role of astrocytes

  • As our preliminary study showed that coxsackievirus receptor (CAR) was expressed on murine astrocytes, we hypothesized that CVB3 infection process in the central nervous system (CNS) involves astrocytes

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Summary

Introduction

Coxsackievirus commonly infects children and occasionally causes severe meningitis and/or encephalitis in the newborn. The underlying mechanism(s) behind the central nervous system pathology is poorly defined. Most coxsackievirus infections are mild, serious complications such as meningitis, paralysis and myocarditis are not rare. Coxsackievirus B3 (CVB3) is the most frequently involved in human myocarditis. Neuroinflammation and neuronal loss have been shown in the central nervous system (CNS) infected by CVB3. Using a neonatal mouse model of CVB3 infection, a previous study has shown that neuronal precursor cells were preferentially targeted and ensuing neuronal apoptosis [3]. Microglia and astrocytes are the major immune cells of the CNS. Our preliminary study showed that microglia were spared from CVB3 infection (unpublished data), whereas the role of astrocytes

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