Pathogenesis and Molecular Biology of HSV Latency and Ocular Reactivation in the Rabbit

Research on herpesvirus infections has commanded the attention of a diverse group of scientists for over a century. Until the advent of the human immunodeficiency virus, the herpes simplex viruses (HSV) were the most intensively studied of all viruses. During the early part of the nineteenth century, long before the infectious agent responsible for cold sores (fever blisters) was identified, studies suggested that damage to the trigeminal nerve could induce peripheral herpetic vesicles (1). Gruter demonstrated that a particle of material from a herpetic blister inoculated into a rabbit eye could cause herpes and that, in this way, the disease could be transmitted in series from one rabbit to another (2). Following Gruter's basic discovery, research conducted in many parts of the world showed a variety of clinical forms of herpes to be similarly transmissible by inoculation (3). At roughly the same time, Goodpasture proposed that "the virus remains in the ganglia in a latent state after the local lesion has healed" and discussed in detail the pathology of herpetic infection in humans and animals (4,5).