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本文引用的文献

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Enhancer requirement for murine cytomegalovirus growth and genetic complementation by the human cytomegalovirus enhancer.小鼠巨细胞病毒生长对增强子的需求以及人巨细胞病毒增强子的基因互补作用
J Virol. 1998 Nov;72(11):8502-9. doi: 10.1128/JVI.72.11.8502-8509.1998.
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Virus attenuation after deletion of the cytomegalovirus Fc receptor gene is not due to antibody control.巨细胞病毒Fc受体基因缺失后的病毒减毒并非由于抗体控制。
J Virol. 1998 Feb;72(2):1377-82. doi: 10.1128/JVI.72.2.1377-1382.1998.
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Cloning and mutagenesis of a herpesvirus genome as an infectious bacterial artificial chromosome.作为一种感染性细菌人工染色体的疱疹病毒基因组的克隆与诱变
Proc Natl Acad Sci U S A. 1997 Dec 23;94(26):14759-63. doi: 10.1073/pnas.94.26.14759.
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Inhibition of natural killer cells by a cytomegalovirus MHC class I homologue in vivo.巨细胞病毒MHC I类同源物在体内对自然杀伤细胞的抑制作用。
Nature. 1997 Apr 3;386(6624):510-4. doi: 10.1038/386510a0.
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Analysis of the complete DNA sequence of murine cytomegalovirus.小鼠巨细胞病毒全DNA序列分析
J Virol. 1996 Dec;70(12):8833-49. doi: 10.1128/JVI.70.12.8833-8849.1996.
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Defined large-scale alterations of the human cytomegalovirus genome constructed by cotransfection of overlapping cosmids.通过共转染重叠黏粒构建的人巨细胞病毒基因组的大规模特定改变。
J Virol. 1996 Mar;70(3):2044-8. doi: 10.1128/JVI.70.3.2044-2048.1996.
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Murine cytomegalovirus with a deletion of genes spanning HindIII-J and -I displays altered cell and tissue tropism.缺失跨越HindIII-J和-I基因的小鼠巨细胞病毒表现出改变的细胞和组织嗜性。
J Virol. 1996 Mar;70(3):1365-74. doi: 10.1128/JVI.70.3.1365-1374.1996.
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Packaging capacity and stability of human adenovirus type 5 vectors.5型人腺病毒载体的包装能力和稳定性
J Virol. 1993 Oct;67(10):5911-21. doi: 10.1128/JVI.67.10.5911-5921.1993.
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The conditions of primary infection define the load of latent viral genome in organs and the risk of recurrent cytomegalovirus disease.原发性感染的情况决定了器官中潜伏病毒基因组的负荷以及巨细胞病毒复发疾病的风险。
J Exp Med. 1994 Jan 1;179(1):185-93. doi: 10.1084/jem.179.1.185.
10
Genes in the HindIII J fragment of the murine cytomegalovirus genome are dispensable for growth in cultured cells: insertion mutagenesis with a lacZ/gpt cassette.小鼠巨细胞病毒基因组HindIII J片段中的基因对于在培养细胞中的生长并非必需:利用lacZ/gpt盒进行插入诱变
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在病毒重建过程中从BAC克隆的疱疹病毒基因组中系统切除载体序列。

Systematic excision of vector sequences from the BAC-cloned herpesvirus genome during virus reconstitution.

作者信息

Wagner M, Jonjic S, Koszinowski U H, Messerle M

机构信息

Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Ludwig-Maximilians-Universität München, D-81377 Munich, Germany.

出版信息

J Virol. 1999 Aug;73(8):7056-60. doi: 10.1128/JVI.73.8.7056-7060.1999.

DOI:10.1128/JVI.73.8.7056-7060.1999
PMID:10400809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC112796/
Abstract

Recently the mouse cytomegalovirus (MCMV) genome was cloned as an infectious bacterial artificial chromosome (BAC) (M. Messerle, I. Crnkovic, W. Hammerschmidt, H. Ziegler, and U. H. Koszinowski, Proc. Natl. Acad. Sci. USA 94:14759-14763, 1997). The virus obtained from this construct is attenuated in vivo due to deletion of viral sequences and insertion of the BAC vector. We reconstituted the full-length MCMV genome and flanked the BAC vector with identical viral sequences. This new construct represents a versatile basis for construction of MCMV mutants since virus generated from the construct loses the bacterial sequences and acquires wild-type properties.

摘要

最近,小鼠巨细胞病毒(MCMV)基因组被克隆为一种感染性细菌人工染色体(BAC)(M. 梅塞尔勒、I. 克尔恩科维奇、W. 哈默施密特、H. 齐格勒和U. H. 科斯齐诺夫斯基,《美国国家科学院院刊》94:14759 - 14763,1997年)。由于病毒序列的缺失和BAC载体的插入,从该构建体获得的病毒在体内减毒。我们重构了全长MCMV基因组,并在BAC载体两侧加上相同的病毒序列。这种新的构建体是构建MCMV突变体的通用基础,因为从该构建体产生的病毒会丢失细菌序列并获得野生型特性。