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一种单纯疱疹病毒1型变体(1720)产生四种等摩尔异构体,尽管从TRL缺失了9200个碱基对,并且9200个核苷酸与97,000个核苷酸之间的序列以反向排列与94,000 - 126,372个核苷酸的序列共价结合。

A HSV-1 variant (1720) generates four equimolar isomers despite a 9200-bp deletion from TRL and sequences between 9200 np and 97,000 np in inverted orientation being covalently bound to sequences 94,000-126,372 np.

作者信息

Harland J, Brown S M

机构信息

MRC Virology Unit, Institute of Virology, Glasgow, UK.

出版信息

Virus Genes. 1992 Aug;6(3):291-9. doi: 10.1007/BF01702567.

DOI:10.1007/BF01702567
PMID:1329342
Abstract

The genome structure of a spontaneously generated HSV-1 strain 17 variant, 1720, has been determined by restriction endonuclease and Southern blot analysis. The short segment of 1720 is unaltered compared to the parental strain 17 genome, whereas the long segment is extensively rearranged. Almost all of TRL (approximately 9.2 kb) has been deleted and consequently IRL is converted into unique sequence. Sequences from approximately 9200 nucleotide position (np) to 97,000 np are present in inverted orientation, covalently bound to sequences in the prototype orientation from approximately 94,000 np to the L/S junction at 126,372 np. Thus, sequences from 94,000 np to 97,000 np are now diploid, with one copy in the normal orientation and location, and the other at the long terminus as an inverted repeat; no inversion of the intervening unique sequences occurs about this novel inverted repeat. In contrast, normal inversions of the long and short segments occur to give four equimolar genomic isomers, indicating that the novel long terminus has gained an "a" sequence. The duplication of sequences between 94,000 np and 97,000 np results in a genome containing two copies of UL43 and one complete and one partial copy each of genes UL42 and UL44 encoding the 65 kD DNA-binding protein and glycoprotein C, respectively. The variant has been shown to grow normally in vitro following high multiplicity infection.

摘要

通过限制性内切酶和Southern印迹分析,已确定自发产生的单纯疱疹病毒1型(HSV-1)菌株17的变体1720的基因组结构。与亲本菌株17基因组相比,1720的短片段未发生改变,而长片段则发生了广泛重排。几乎所有的TRL(约9.2 kb)已被删除,因此IRL转化为独特序列。从大约9200核苷酸位置(np)到97,000 np的序列以反向排列存在,与从大约94,000 np到126,372 np处的L/S连接处的原型方向的序列共价结合。因此,从94,000 np到97,000 np的序列现在是二倍体,一个拷贝处于正常方向和位置,另一个作为反向重复序列位于长末端;围绕这个新的反向重复序列,中间的独特序列没有发生倒位。相比之下,长片段和短片段发生正常倒位,产生四种等摩尔的基因组异构体,表明新的长末端获得了一个“a”序列。94,000 np和97,000 np之间序列的重复导致基因组包含两个UL43拷贝,以及分别编码65 kD DNA结合蛋白和糖蛋白C的基因UL42和UL44的一个完整拷贝和一个部分拷贝。已证明该变体在高 multiplicity感染后在体外能正常生长。

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1
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Virus Genes. 1992 Aug;6(3):291-9. doi: 10.1007/BF01702567.
2
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引用本文的文献

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Machinery to support genome segment inversion exists in a herpesvirus which does not naturally contain invertible elements.支持基因组片段倒位的机制存在于一种天然不包含可倒位元件的疱疹病毒中。
J Virol. 2000 May;74(10):4882-7. doi: 10.1128/jvi.74.10.4882-4887.2000.

本文引用的文献

1
Detailed analysis of the portion of the herpes simplex virus type 1 genome encoding glycoprotein C.对1型单纯疱疹病毒基因组中编码糖蛋白C的部分进行详细分析。
J Virol. 1983 Feb;45(2):634-47. doi: 10.1128/JVI.45.2.634-647.1983.
2
Site-specific inversion sequence of the herpes simplex virus genome: domain and structural features.单纯疱疹病毒基因组的位点特异性倒位序列:结构域和结构特征
Proc Natl Acad Sci U S A. 1981 Nov;78(11):7047-51. doi: 10.1073/pnas.78.11.7047.
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One functional copy of the long terminal repeat gene specifying the immediate-early polypeptide IE 110 suffices for a productive infection of human foetal lung cells by herpes simplex virus.
J Gen Virol. 1981 Jul;55(Pt 1):179-91. doi: 10.1099/0022-1317-55-1-179.
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Nucleotide sequences of the joint between the L and S segments of herpes simplex virus types 1 and 2.单纯疱疹病毒1型和2型L与S片段连接处的核苷酸序列。
J Gen Virol. 1981 Aug;55(Pt 2):315-31. doi: 10.1099/0022-1317-55-2-315.
5
Molecular engineering of the herpes simplex virus genome: insertion of a second L-S junction into the genome causes additional genome inversions.单纯疱疹病毒基因组的分子工程:在基因组中插入第二个L-S连接会导致额外的基因组倒位。
Cell. 1980 Nov;22(1 Pt 1):243-55. doi: 10.1016/0092-8674(80)90172-5.
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A herpes simplex virus type 1 variant which fails to synthesize immediate early polypeptide VmwIE63.一种无法合成立即早期多肽VmwIE63的1型单纯疱疹病毒变体。
J Gen Virol. 1987 May;68 ( Pt 5):1339-50. doi: 10.1099/0022-1317-68-5-1339.
7
Three mutants of herpes simplex virus type 2: one lacking the genes US10, US11 and US12 and two in which Rs has been extended by 6 kb to 0.91 map units with loss of Us sequences between 0.94 and the Us/TRs junction.2型单纯疱疹病毒的三个突变体:一个缺失US10、US11和US12基因,另外两个中Rs已延伸6 kb至0.91个图距单位,在0.94与Us/TRs连接处之间的Us序列缺失。
J Gen Virol. 1987 Jan;68 ( Pt 1):1-18. doi: 10.1099/0022-1317-68-1-1.
8
Functional domains within the a sequence involved in the cleavage-packaging of herpes simplex virus DNA.单纯疱疹病毒DNA切割包装过程中涉及的α序列内的功能结构域。
J Virol. 1986 Sep;59(3):605-18. doi: 10.1128/JVI.59.3.605-618.1986.
9
Herpes simplex virus amplicon: cleavage of concatemeric DNA is linked to packaging and involves amplification of the terminally reiterated a sequence.单纯疱疹病毒扩增子:串联DNA的切割与包装相关,并涉及末端重复a序列的扩增。
J Virol. 1986 Mar;57(3):933-41. doi: 10.1128/JVI.57.3.933-941.1986.
10
Isolation and characterization of deletion mutants of herpes simplex virus type 2 (strain HG52).2型单纯疱疹病毒(HG52株)缺失突变体的分离与鉴定
J Gen Virol. 1985 Jun;66 ( Pt 6):1305-21. doi: 10.1099/0022-1317-66-6-1305.