文档介绍：
Induction of cytopathic effect and cytokines in
coxsackievirus B3-infected murine astrocytes#
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ZENG Jun, WANG Gefei, LI Weizhong, CHEN Xiaoxuan, XIN Gang,
ZHANG Dangui, JIANG Zhiwu, LI Kangsheng**
(Department of Immunology and Microbiology, Shantou University Medical College,
GuangDong ShanTou 515041)
Abstract: monly 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. It 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. CVB3 infected and replicated in
astrocytes, with release of infectious virus particles. CVB3 induced cytopathic effect (CPE) and
production of proinflammatory cytokines IL-1β, TNF-α, IL-6, and chemokine CXCL10 from astrocytes.
These data suggest that direct astrocyte damage and cytokines induction could be a mechanism of
virus-induced neuropathology.
Keywords: viral infection; coxsackievirus; astrocyte; cell death; cytokine; neuroinflammation
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Introduction
Coxsackieviruses are important human pathogens. Although most coxsackievirus infections
are mild, plications such as meningitis, paralysis and myocarditis are not rare.
Coxsackievirus B3 (CVB3) is the most frequently involved in human myocarditis. Recently,
increasing cases of CVB3-associated meningitis have been reported. Neuroinflammation and
neuronal loss have been shown in the central nervous system (CNS) infected by CVB3. Using a
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neonatal mouse model of CVB3 infection, a previous study has shown that neuronal precursor
cells were preferentially targeted and ensuing neuronal apoptosis. Microglia and astrocytes are the
major immune cells of S. Our preliminary study showed that microglia were spared from
CVB3 infection, wherea