HSV1 ICPO AND REACTIVATION FROM LATENCY

1型单纯疱疹病毒（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。 虽然大量的间接证据表明， HSV-1反式激活因子）在再激活、直接激活和免疫抑制中起核心作用。 缺乏支持这一假设的证据。 的限制因素 ICPO突变体体内研究（与许多其它HSV-1突变体一样） ICPO突变体的复制效率不如野生型 动物中的HSV-1因此，从以前的分析中还不清楚， 三叉神经瘤ICPO突变病毒的再活化减少， 神经节是由于低效的神经元定植和潜伏的 感染，或在HSV-1再活化中需要ICPO。 的目标 本文提出的研究是a）开发方法， 在小鼠中用突变型和野生型HSV-1建立相等的潜伏期， 并使用这些方法B）获得明确的证据，以支持 或拒绝ICPO在HSV-1再活化中起作用的假设。

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.