How herpesviruses sense stress in their hosts

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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.