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An electron-microscopic study of avirulent and virulent Semliki forest virus in the brains of different ages of mice.

作者信息

Pathak S, Webb H E

出版信息

J Neurol Sci. 1978 Dec;39(2-3):199-211. doi: 10.1016/0022-510x(78)90123-5.

DOI:10.1016/0022-510x(78)90123-5
PMID:739267
Abstract

Ultrastructural studies of brains infected with avirulent and virulent strains of Semliki forest virus (SFV) were performed in 2-7, 14, 19, and 21-28 day old mice. Mature virus particles, dense clumps of fine granules, spherules and advanced stages of viral development i.e. cytopathic vacuoles, Type II (CPV II) are seen in the brains at all ages with the virulent strain which is pathogenic to all age group of mice. In the avirulent strain infection which is pathogenic to mice below 15 days old, no mature virus particles or advanced stages of viral development are seen in 19 day old and adult mice in spite of high virus titres. However, dense clumps of fine granules and spherules are seen which seem to have the capacity to develop into lethal highly infectious mature virus when reinoculated into 2-7 day old mice. It is suggested that the dense clumps of fine granules and spherules are very early viral forms, which are seen in all age groups of mice. The cut-off mechanism in pathogenicity of the avirulent strain occurs in mice around 14 days old. Though some mature virus particles and advanced viral developmental stages are seen in these mice they were much less frequent compared to baby mice. Lymphoblastic type cells are numerous in this age group. These cells are seen more frequently in all ages of mice infected with the avirulent strain as compared to the virulent strain. These mononuclear cells can have an immunological role and may play a part in limiting the process of viral maturation and hence preventing death. Polymorphs and macrophages are rare with the avirulent infection but are the predominant infiltrating cells in the virulent strain infections. With the avirulent infections the astrocytes show hypertrophy and intranuclear inclusions are seen in them.

摘要

相似文献

1
An electron-microscopic study of avirulent and virulent Semliki forest virus in the brains of different ages of mice.
J Neurol Sci. 1978 Dec;39(2-3):199-211. doi: 10.1016/0022-510x(78)90123-5.
2
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引用本文的文献

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Pseudo-typed Semliki Forest virus delivers EGFP into neurons.假型塞姆利基森林病毒将增强绿色荧光蛋白递送至神经元中。
J Neurovirol. 2017 Apr;23(2):205-215. doi: 10.1007/s13365-016-0486-8. Epub 2016 Oct 13.
2
Semliki Forest virus A7(74) transduces hippocampal neurons and glial cells in a temperature-dependent dual manner.塞姆利基森林病毒A7(74)以温度依赖性双重方式转导海马神经元和神经胶质细胞。
J Neurovirol. 2003 Feb;9(1):16-28. doi: 10.1080/13550280390173346.
3
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.
4
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.
5
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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Oligodendrocyte infection and demyelination produced in mice by the M9 mutant of Semliki Forest virus.由塞姆利基森林病毒M9突变体在小鼠中引发的少突胶质细胞感染和脱髓鞘病变。
Acta Neuropathol. 1983;60(3-4):257-65. doi: 10.1007/BF00691874.
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Lysosomal enzyme changes in macrophages from mice given myocrisin and infected with avirulent Semliki Forest virus.给予金诺芬并感染无毒力的Semliki森林病毒的小鼠巨噬细胞中溶酶体酶的变化。
Br J Exp Pathol. 1982 Aug;63(4):443-6.
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Demyelination in mice resulting from infection with a mutant of Semliki Forest virus.感染塞姆利基森林病毒突变体导致小鼠脱髓鞘。
Acta Neuropathol. 1981;53(2):129-36. doi: 10.1007/BF00689993.