HSV1 ICPO AND REACTIVATION FROM LATENCY

单纯疱疹病毒1型(HSV-1)重新激活的过程 从潜伏期到引起复发性疱疹疾病的定义不明确。 尽管相当多的间接证据表明ICPO(一个 HSV-1反式激活因子)在重新激活中起核心作用，直接 缺乏支持这一假设的证据。一个限制因素 在体内对ICPO突变体的研究(与许多其他HSV-1突变体一样) 因为ICPO突变体的复制效率不如野生型 动物体内的HSV-1。因此，从之前的分析来看，尚不清楚 三叉神经来源的ICPO突变病毒的再激活减少 神经节是由于低效的神经元定植和潜伏 感染，或在HSV-1重新激活过程中需要ICPO。目标 本文建议的研究之一是a)开发方法，使 在小鼠体内建立与突变型和野生型HSV-1相同的潜伏期， 并使用这些方法b)获得确凿的证据来支持 或者拒绝ICPO在HSV-1重新激活中起作用的假设。

The process by which herpes simplex virus type 1 (HSV-1) reactivates from latency to cause recurrent herpetic disease is poorly defined. Although considerable circumstantial evidence suggests that ICPO (an HSV-1 transactivator) plays a central role in reactivation, direct evidence to support this hypothesis is lacking. A limiting factor in the study of ICPO mutants in vivo (as with many other HSV-1 mutants) has been that ICPO mutants do not replicate as efficiently as wild-type HSV-1 in animals. Consequently, it is unclear from previous analyses if the decreased reactivation of ICPO- mutant viruses from trigeminal ganglion is due to inefficient neuronal colonization and latent infection, or a requirement for ICPO in HSV-1 reactivation. The goals of the studies proposed herein is to a) develop methods that allow the equal establishment of latency with mutant and wild-type HSV-1 in mice, and using these methods b) obtain definitive evidence to either support or reject the hypothesis that ICPO plays a role in HSV-1 reactivation.