Synergism between the components of the bipartite major immediate-early transcriptional enhancer of murine cytomegalovirus does not accelerate virus replication in cell culture and host tissues.
Synergism between the components of the bipartite major immediate-early transcriptional enhancer of murine cytomegalovirus does not accelerate virus replication in cell culture and host tissues.
复制标题
鼠巨细胞病毒二部分主要立即早期转录增强子的组分之间的协同作用不会加速病毒在细胞培养物和宿主组织中的复制。
DOI：
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发表时间：
2009
影响因子：
3.8
通讯作者：
N. K. Grzimek
中科院分区：
文献类型：
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作者：
Kai A. Kropp;Christian O. Simon;Annette Fink;Angélique Renzaho;Birgit Kühnapfel;J. Podlech;M. Reddehase;N. K. Grzimek
巨细胞病毒的主要即刻早期(MIE)转录增强子是被认为是病毒复制适合性和致病性的决定因素的关键调节因子。小鼠巨细胞病毒(MCMV)的MIE基因座具有双向基因对结构，其两侧是一个由不同核心启动子组成的两段增强子。在这里，我们构建了重组病毒MCMV-DeltaEnh1和MCMV-DeltaEnh2，以研究其中一个增强子成分对MIE基因双向转录的影响，以及对细胞培养和与CMV病相关的各种宿主组织中病毒复制的影响。数据显示，两个单链增强子可以独立作用，但在感染后早期协同增强MIE基因的表达。然而，由两部分增强子配置促进的启动转录最终并没有导致病毒复制的加速。我们得出的结论是，一旦被触发，病毒复制就以固定的速度进行，我们认为两部分增强子组件之间的协同作用可能会增加转录启动的可能性。
Major immediate-early (MIE) transcriptional enhancers of cytomegaloviruses are key regulators that are regarded as determinants of virus replicative fitness and pathogenicity. The MIE locus of murine cytomegalovirus (mCMV) shows bidirectional gene-pair architecture, with a bipartite enhancer flanked by divergent core promoters. Here, we have constructed recombinant viruses mCMV-DeltaEnh1 and mCMV-DeltaEnh2 to study the impact of either enhancer component on bidirectional MIE gene transcription and on virus replication in cell culture and various host tissues that are relevant to CMV disease. The data revealed that the two unipartite enhancers can operate independently, but synergize in enhancing MIE gene expression early after infection. Kick-start transcription facilitated by the bipartite enhancer configuration, however, did not ultimately result in accelerated virus replication. We conclude that virus replication, once triggered, proceeds with a fixed speed and we propose that synergism between the components of the bipartite enhancer may rather increase the probability for transcription initiation.