Nuclear localization of the C1 factor (host cell factor) in sensory neurons correlates with reactivation of herpes simplex virus from latency
Nuclear localization of the C1 factor (host cell factor) in sensory neurons correlates with reactivation of herpes simplex virus from latency
复制标题
DOI：
10.1073/pnas.96.4.1229
复制
发表时间：
1999-02-16
影响因子：
11.1
通讯作者：
Sears, AE
中科院分区：
文献类型：
--
作者：
Kristie, TM;Vogel, JL;Sears, AE
初次感染后，单纯疱疹病毒在感觉神经节的神经元中保持潜伏状态，直到复杂的刺激重新激活病毒裂解复制。尽管控制从潜伏状态重新激活的机制仍然未知，但病毒立即早期基因的调节表达代表了这一过程中的关键点。这些基因由转录增强子复合物控制，其组装需要细胞 C1 因子（宿主细胞因子）并由其协调。与其他组织相比，感觉神经元的细胞核中未检测到 C1 因子。在小鼠模型系统中诱导单纯疱疹病毒重新激活的实验条件导致蛋白质快速核定位，表明C1因子被隔离在这些细胞中，直到重新激活信号诱导蛋白质重新分布。受调控的定位表明 C1 是病毒裂解潜伏周期的关键开关决定因素。
After a primary infection, herpes simplex virus is maintained in a latent state in neurons of sensory ganglia until complex stimuli reactivate viral lytic replication. Although the mechanisms governing reactivation from the latent state remain unknown, the regulated expression of the viral immediate early genes represents a critical point in this process. These genes are controlled by transcription enhancer complexes whose assembly requires and is coordinated by the cellular C1 factor (host cell factor). In contrast to other tissues, the C1 factor is not detected in the nuclei of sensory neurons. Experimental conditions that induce the reactivation of herpes simplex virus in mouse model systems result in rapid nuclear localization of the protein, indicating that the C1 factor is sequestered in these cells until reactivation signals induce a redistribution of the protein. The regulated localization suggests that C1 is a critical switch determinant of the viral lytic-latent cycle.