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对塞姆利基森林病毒强毒株和无毒株在小鼠脑中发育情况的电子显微镜研究。

An electron-microscopic study of the development of virulent and avirulent strains of Semliki forest virus in mouse brain.

作者信息

Pathak S, Webb H E, Oaten S W, Bateman S

出版信息

J Neurol Sci. 1976 Jul;28(3):289-300. doi: 10.1016/0022-510x(76)90022-8.

DOI:10.1016/0022-510x(76)90022-8
PMID:932776
Abstract

Two strains of Semliki Forest Virus (SFV), the avirulent and virulent, were used to study the development of virus in both baby and adult mouse brain. The development of SFV in the brain was similar in baby and adult brain using the virulent strain and in the baby mouse brain using the avirulent strain. Mature virus could not be found in adult mouse brain using the avirulent strain. This paper shows that extracellular virus particles near the cell membrane stimulate the formation of coated vesicles and thus absorption of virus particles by the cell. It is suggested that these coated vesicles with contained virus particles are stimulated to develop nucleoid cores on their membrane forming cytopathic vacuoles, Type II (CPV-II). Excessive membrane growth takes place and the membrane of the CPV-II with the nucleoid cores invaginates to form intravacuolar tubules. It is suggested that these tubules become responsible fro the formation of mature virus particles. Thus the membrane of the CPV-II appears to be responsible for the development of both the inner core and outer coat of the virus.

摘要

使用两种株系的塞姆利基森林病毒(SFV),即无毒株和有毒株,来研究病毒在幼鼠和成年鼠大脑中的发育情况。使用有毒株时,SFV在幼鼠和成年鼠大脑中的发育情况相似;使用无毒株时,SFV在幼鼠大脑中的发育情况也是如此。使用无毒株时,在成年鼠大脑中未发现成熟病毒。本文表明,细胞膜附近的细胞外病毒颗粒刺激包被小泡的形成,从而促使细胞吸收病毒颗粒。有人提出,这些含有病毒颗粒的包被小泡会被刺激在其膜上形成核样核心,进而形成II型细胞病变空泡(CPV-II)。会发生过度的膜生长,带有核样核心的CPV-II的膜内陷形成泡内小管。有人提出,这些小管负责成熟病毒颗粒的形成。因此,CPV-II的膜似乎负责病毒内核和外壳的形成。

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引用本文的文献

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A novel neurotropic expression vector based on the avirulent A7(74) strain of Semliki Forest virus.一种基于减毒的塞姆利基森林病毒A7(74)株的新型嗜神经表达载体。
J Neurovirol. 2003 Feb;9(1):1-15. doi: 10.1080/13550280390173382.
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bcl-2 acts early to restrict Semliki Forest virus replication and delays virus-induced programmed cell death.
bcl-2早期发挥作用,限制Semliki森林病毒复制,并延缓病毒诱导的程序性细胞死亡。
J Virol. 1997 Feb;71(2):1583-90. doi: 10.1128/JVI.71.2.1583-1590.1997.
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Pathogenesis of virus-induced demyelination.病毒诱导的脱髓鞘病变的发病机制。
Adv Virus Res. 1993;42:249-324. doi: 10.1016/s0065-3527(08)60087-1.
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In vivo depletion of CD8+ T cells prevents lesions of demyelination in Semliki Forest virus infection.体内清除CD8 + T细胞可预防塞姆利基森林病毒感染中的脱髓鞘病变。
J Virol. 1993 Dec;67(12):7629-33. doi: 10.1128/JVI.67.12.7629-7633.1993.
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On the entry of Semliki forest virus into BHK-21 cells.关于Semliki森林病毒进入BHK - 21细胞的过程。
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