Ocular infections with herpes simplex virus(HSV) in humans vary in clinical manifestation ranging from self limiting benign epithelial disease to nectrotizing stromal keratitis and uveitis. A . serious clinical problem is the recurrence of ocular lesions due to reactivation of latent virus from dorsal root ganglia. The rabbit eye has provided an efficient experimental model system for study of the mechanisms underlying herpes virus keratitis and the various factors affecting the establishment, maintenance and reactivation of latent HSV. The work described in this thesis stems from the observations of Gerdes and Smith(1983) who showed that in the rabbit eye model, spontaneous shedding of HSV following ocular infection and establishment of a latent infection in the trigeminal ganglia, is virus strain specific and the virus genes controlling reactivation are different from those needed for the establishment and maintenance of HSV latency.