How herpesviruses sense stress in their hosts

疱疹病毒（人类单纯疱疹病毒，HSV-1就是一个例子）的感染开始于病毒在皮肤细胞中进入部位的活跃复制。然后病毒感染支配病毒复制区域的感觉神经，并在神经细胞中建立潜伏感染。它静静地呆在这里，免受宿主的防御。神经细胞中的潜伏病毒对环境或生理压力的反应是周期性地重新激活，复制并重新感染皮肤细胞。潜伏期建立的分子基础长期以来一直是病毒学家的一个有趣和令人困惑的难题，一个尚未解决的难题。我们研究的目的是确定HSV-1在宿主受到压力时的感觉。我们的工作不仅将帮助我们了解疱疹病毒如何建立潜伏期并从中重新激活，还将告诉我们神经系统细胞如何对压力做出反应。

Infection with a herpesvirus (the human herpes simplex virus, HSV-1 is an example) begins with active replication of the virus in skin cells at the site of entry. The virus then infects sensory nerves innervating the area of virus replication and establishes a latent infection in nerve cells. Here it quietly remains, protected from the host's defenses. In response to environmental or physiological stress the latent virus in nerve cells reactivates periodically to replicate and reinfect skin cells. The molecular basis for the establishment of latency has long been an intriguing and perplexing puzzle for virologists, a puzzle that has not as yet been solved. The objective of our research is to determine how HSV-1 senses when its host is stressed. Our work will not only help us to understand how herpesviruses establish latency and reactivate from it, it will also tell us how cells of the nervous system respond to stress.