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本文引用的文献

1
Severity of experimentally reactivated herpetic eye disease is related to the neurovirulence of the latent virus.实验性重新激活的疱疹性眼病的严重程度与潜伏病毒的神经毒性有关。
Invest Ophthalmol Vis Sci. 1987 Feb;28(2):229-37.
2
Neuropathology of herpes simplex virus encephalitis in a rat seizure model.大鼠癫痫模型中单纯疱疹病毒性脑炎的神经病理学
J Neuropathol Exp Neurol. 1993 May;52(3):241-52. doi: 10.1097/00005072-199305000-00008.
3
Herpes simplex virus type 1 strain KOS-63 does not cause acute or recurrent ocular disease and does not reactivate ganglionic latency in vivo.
单纯疱疹病毒1型KOS-63株不会引起急性或复发性眼部疾病,且在体内不会激活神经节潜伏状态。
Acta Neuropathol. 1994;87(1):14-22. doi: 10.1007/BF00386250.
4
Herpes simplex encephalitis in the temporal cortex and limbic system after trigeminal nerve inoculation.三叉神经接种后颞叶皮质和边缘系统的单纯疱疹性脑炎。
J Infect Dis. 1994 Apr;169(4):782-6. doi: 10.1093/infdis/169.4.782.
5
A thymidine kinase deficient HSV-2 strain causes acute keratitis and establishes trigeminal ganglionic latency, but poorly reactivates in vivo.一种胸苷激酶缺陷型单纯疱疹病毒2型毒株可引起急性角膜炎并建立三叉神经节潜伏感染,但在体内再激活能力较差。
J Med Virol. 1994 Jul;43(3):297-309. doi: 10.1002/jmv.1890430319.
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Genomic sequencing.基因组测序
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7
Physical location of a herpes simplex virus type-1 gene function(s) specifically associated with a 10 million-fold increase in HSV neurovirulence.单纯疱疹病毒1型基因功能的物理定位,该功能与HSV神经毒力增加1000万倍特别相关。
Virology. 1983 Nov;131(1):180-92. doi: 10.1016/0042-6822(83)90544-5.
8
Biological characterization of a herpes simplex virus intertypic recombinant which is completely and specifically non-neurovirulent.一种完全且特异性无神经毒性的单纯疱疹病毒型间重组体的生物学特性
Virology. 1983 Nov;131(1):171-9. doi: 10.1016/0042-6822(83)90543-3.
9
HSV-1 thymidine kinase promotes virulence and latency in the mouse.
Invest Ophthalmol Vis Sci. 1983 May;24(5):599-602.
10
Comparative neurovirulence of herpes simplex virus type 1 strains after peripheral or intracerebral inoculation of BALB/c mice.1型单纯疱疹病毒株经外周或脑内接种BALB/c小鼠后的比较神经毒力
Infect Immun. 1983 Apr;40(1):103-12. doi: 10.1128/iai.40.1.103-112.1983.

单纯疱疹病毒1型毒株H129和+GC的克隆及限制性内切酶图谱分析

Cloning and restriction endonuclease mapping of herpes simplex virus type-1 strains H129 and +GC.

作者信息

Kienzle T E, Henkel J S, Ling J Y, Banks M C, Beers D R, Jones B, Stroop W G

机构信息

John McClellan Veterans Affairs Medical Center, Little Rock, Arkansas, USA.

出版信息

Arch Virol. 1995;140(9):1663-75. doi: 10.1007/BF01322540.

DOI:10.1007/BF01322540
PMID:7487498
Abstract

EcoRI fragments of herpes simplex virus I (HSV-1) strains H129 and +GC were cloned and the EcoRI and BglII restriction enzyme sites were mapped. Comparison of these enzyme sites with the sequence of HSV-1 strain 17syn+ demonstrated that all EcoRI sites were identical. For H129, the BglII sites were also found to match strain 17syn+ BglII sites. With one exception, the BglII sites in strain +GC also aligned with the strain 17syn+ sequence. The one exception was a missing BglII site from strain +GC located between bases 25,149 and 25,154 in the EcoRI D fragment within the viral deoxyribonuclease gene (UL12). The BglII site represents the first difference to be mapped within HSV-1 strains H129 and +GC which have unique pathobiological properties in animal models of acute and reactivated infections.

摘要

克隆了单纯疱疹病毒I型(HSV-1)毒株H129和+GC的EcoRI片段,并绘制了EcoRI和BglII限制性酶切位点图谱。将这些酶切位点与HSV-1毒株17syn+的序列进行比较,结果表明所有EcoRI位点均相同。对于H129,还发现其BglII位点与毒株17syn+的BglII位点匹配。除了一个例外,+GC毒株中的BglII位点也与毒株17syn+的序列一致。这个例外是+GC毒株在病毒脱氧核糖核酸酶基因(UL12)的EcoRI D片段中位于第25149至25154个碱基之间的一个缺失的BglII位点。该BglII位点是在具有急性和再激活感染动物模型中独特病理生物学特性的HSV-1毒株H129和+GC中绘制出的首个差异位点。