Establishment of latent ganglionic infection with herpes simplex virus via maxillary gingiva and viral re-activation in vivo after trauma.

Herpes simplex virus can remain latent for months or years in sensory and automatic ganglia of animals and man, and can be re-activated in vivo by several procedures such as neurectomy, irritation of epithelial surfaces, and administration of immunosuppressive agents. The objective of this study was to determine whether dental stimuli can cause re-activation of the latent herpes simplex virus. Homogenization and explanation of ganglia from mice showed that herpes simplex virus (type 1) traveled from maxillary gingiva to trigeminal ganglia, and remained latent. It was also shown that mice passively immunized with rabbit antibody to herpes simplex virus, following the inoculation of herpes simplex virus by the maxillary gingiva route, developed a latent infection in the trigeminal ganglia. Neutralizing antibody was cleared from the circulation and could not be detected in most of these animals after five weeks. A neutralizing test showed that antibody-negative mice with latent infection were able to produce antibody to re-infection with herpes simplex virus, suggesting that re-activation can be identified by measurement of serum antibody. By use of this mouse model system, it was shown that when maxillary gingiva was traumatized with dry ice, viral re-activation occurred in 58% of these animals, as demonstrated by the appearance of neutralizing antibody. Irradiation by a Stomalaser beam had no effect on the re-activation of latent herpes simplex virus. Our mouse model system may serve as a useful model for obtaining new information on re-activating or inhibitory factors in dentistry.