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Primary neurons become less susceptible to coxsackievirus B5 following maturation: The correlation with the decreased level of CAR expression on cell surface
Author(s) -
Ahn Jeonghyun,
Jee Youngmee,
Seo Ilseon,
Yoon Seung Yong,
Kim DongHou,
Kim Yoo Kyum,
Lee Heuiran
Publication year - 2008
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.21100
Subject(s) - coxsackievirus , biology , virology , virus , capsid , receptor , aseptic meningitis , antibody , virulence , central nervous system , cytopathic effect , immunology , enterovirus , gene , genetics , cerebrospinal fluid , neuroscience
Coxsackievirus B (CVB) is one of the major pathogens of aseptic meningitis and meningioencephalitis, particularly in newborn infants. To analyze the influence of neural maturation on susceptibility to CVB infection, we prepared immature and mature neurons from 16‐day‐old BALB/c embryonic cortex. In contrast to immature neurons, mature neurons were less susceptible to CVB5 infection, as indicated by the decrease of cytopathic features. In mature neurons, progeny virus production was significantly hindered, and virus capsid protein VP1 synthesis and virus genome amplification were concomitantly reduced. In addition, the expression of coxsackievirus and adenovirus receptor (CAR), the major receptor of CVB5, was down‐regulated in mature neurons. The antibody treatment specific to CAR significantly attenuated CVB5 susceptibility of immature neurons. These findings demonstrate that mature neurons become less susceptible to CVB by the decrease of CAR level. Thus, the data strongly support the idea that the level of virus receptor in neurons is one of the crucial determinants in the age‐dependency of CVB virulence in central nervous system. J. Med. Virol. 80:434–440, 2008. © 2008 Wiley‐Liss, Inc.