ABSTRACT
Herpes simplex virus (HSV) is the most common cause of monocular infectious blindness in the industrialized world and is second only to trachoma in the developing world (1). During the initial infection in the ocular or facial area, HSV replicates in the mucous membranes of the mouth or the corneal epithelium, where sensory and autonomic nerve terminals take up the virus. The virus is transported in a retrograde direction to sensory trigeminal ganglion cell bodies. Although many ganglion neurons support a lytic infection, a subpopulation of neurons supports an HSV infection in which the virus remains latent. The second phase of corneal infection follows from viral reactivation in the latently infected trigeminal ganglion cells. After anterograde transport to the eye, the new virus can be found in tears and in the corneal epithelium and stroma. With repeated reactivation cycles, the corneal stroma becomes progressively scarred, with resulting decrease in vision and other ocular complications including glaucoma, iritis and cataract, and necrotizing retinitis. The burden of ocular HSV relates primarily to its recurrences that result in corneal scarring and glaucoma; the other complications or other ocular tissue involvement are less common. There is no effective therapy to prevent ocular recurrences and the treatment for active ocular HSV is limited.
