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2-溴-5,6-二氯-1-β-D-呋喃核糖基苯并咪唑核苷对豚鼠巨细胞病毒基因组结构、包装和释放的显著影响。

Dramatic effects of 2-bromo-5,6-dichloro-1-beta-D-ribofuranosyl benzimidazole riboside on the genome structure, packaging, and egress of guinea pig cytomegalovirus.

作者信息

Nixon Daniel E, McVoy Michael A

机构信息

Department of Medicine, Medical College of Virginia Campus of Virginia Commonwealth University, Richmond, Virginia 23298-0163, USA.

出版信息

J Virol. 2004 Feb;78(4):1623-35. doi: 10.1128/jvi.78.4.1623-1635.2004.

Abstract

The halogenated benzimidazoles BDCRB (2-bromo-5,6-dichloro-1-beta-D-riborfuranosyl benzimidazole riboside) and TCRB (2,5,6-trichloro-1-beta-D-riborfuranosyl benzimidazole riboside) were the first compounds shown to inhibit cleavage and packaging of herpesvirus genomes. Both inhibit the formation of unit length human cytomegalovirus (HCMV) genomes by a poorly understood mechanism (M. R. Underwood et al., J. Virol. 72:717-715, 1998; P. M. Krosky et al., J. Virol. 72:4721-4728, 1998). Because the simple genome structure of guinea pig cytomegalovirus (GPCMV) provides a useful model for the study of herpesvirus DNA packaging, we investigated the effects of BDCRB on GPCMV. GPCMV proved to be sensitive to BDCRB (50% inhibitory concentration = 4.7 microM), although somewhat less so than HCMV. In striking contrast to HCMV, however, a dose of BDCRB sufficient to reduce GPCMV titers by 3 logs (50 microM) had no effect on the quantity of GPCMV genomic DNA that was formed in infected cells. Electron microscopy revealed that this DNA was in fact packaged within intranuclear capsids, but these capsids failed to egress from the nucleus and failed to protect the DNA from nuclease digestion. The terminal structure of genomes formed in the presence of BDCRB was also altered. Genomes with ends lacking a terminal repeat at the right end, which normally exist in an equimolar ratio with those having one copy of the repeat at the right end, were selectively eliminated by BDCRB treatment. At the left end, BDCRB treatment appeared to induce heterogeneous truncations such that 2.7 to 4.9 kb of left-end-terminal sequences were missing. These findings suggest that BDCRB induces premature cleavage events that result in truncated genomes packaged within capsids that are permeable to nuclease. Based on these and other observations, we propose a model for duplication of herpesvirus terminal repeats during the cleavage and packaging process that is similar to one proposed for bacteriophage T7 (Y. B. Chung, C. Nardone, and D. C. Hinkle, J. Mol. Biol. 216:939-948, 1990).

摘要

卤代苯并咪唑类化合物BDCRB(2-溴-5,6-二氯-1-β-D-核糖呋喃糖基苯并咪唑核苷)和TCRB(2,5,6-三氯-1-β-D-核糖呋喃糖基苯并咪唑核苷)是最先被证明能抑制疱疹病毒基因组切割和包装的化合物。二者均通过一种尚不清楚的机制抑制单位长度人巨细胞病毒(HCMV)基因组的形成(M. R. Underwood等人,《病毒学杂志》72:717 - 715,1998;P. M. Krosky等人,《病毒学杂志》72:4721 - 4728,1998)。由于豚鼠巨细胞病毒(GPCMV)简单的基因组结构为疱疹病毒DNA包装研究提供了一个有用的模型,我们研究了BDCRB对GPCMV的影响。结果证明GPCMV对BDCRB敏感(50%抑制浓度 = 4.7微摩尔),尽管其敏感性略低于HCMV。然而,与HCMV形成鲜明对比的是,一剂足以使GPCMV滴度降低3个对数(50微摩尔)的BDCRB对感染细胞中形成的GPCMV基因组DNA的量没有影响。电子显微镜显示,这种DNA实际上被包装在核内衣壳中,但这些衣壳无法从细胞核中逸出,也无法保护DNA免受核酸酶消化。在BDCRB存在的情况下形成的基因组的末端结构也发生了改变。右端缺乏末端重复序列的基因组,其通常与右端有一个重复序列拷贝的基因组以等摩尔比存在,经BDCRB处理后被选择性消除。在左端,BDCRB处理似乎诱导了异质性截短,使得左端末端序列缺失2.7至4.9 kb。这些发现表明,BDCRB诱导了过早的切割事件,导致截短的基因组被包装在对核酸酶可渗透的衣壳中。基于这些及其他观察结果,我们提出了一个疱疹病毒末端重复序列在切割和包装过程中复制的模型,该模型类似于为噬菌体T7提出的模型(Y. B. Chung、C. Nardone和D. C. Hinkle,《分子生物学杂志》216:939 - 948,1990)。

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