Abstract

Herpes simplex virus (HSV) is known to be latent in ganglionic neurons. Over the past eight years, a series of reports have described the isolation of HSV after organ culture of human corneas that had been removed in the course of penetrating keratoplasty. None of the corneas showed any clinical signs of active herpetic disease immediately before keratoplasty. Studies in rabbits and mice confirmed that HSV can be recovered from corneas by organ culture long after primary infection has subsided. Recently, sophisticated techniques of molecular biology, such as specific DNA or RNA probes, have been used to detect HSV nucleic acids in the cornea. The crux of the matter is whether the virus recovered from or detected in the cornea is 1) truly latent in cell populations that are nonneuronal; 2) resident in the cornea, replicating at a slow rate; or 3) newly arrived in the cornea following ganglionic reactivation. The evidence suggests that a guarded case can be made for limited HSV latency within corneal cells. HSV corneal latency would allow for reactivation, replication, and the immune response to occur in the absence of ganglionic HSV reactivation. Such a localized phenomenon has not, however, been demonstrated to occur clinically.