SUMMARYNineteen recent isolates and three laboratory strains of herpes simplex virus types I and 2 were tested for their ability to produce clinical signs in mice following intradermal inoculation in the ear. All viruses produced erythema at the inoculation site; this was the most sensitive clinical sign of infection. Virus multiplication in the ear tissue was similar for both types I and 2 up to the fifth day after inoculation but type 2 viruses persisted for longer. Latent infection was demonstrated in cervical dorsal root ganglia. Type I viruses required a much higher dose than type 2 to produce neurological signs and death after intradermal inoculation but the difference was less after intracerebral inoculation.Erythema of the inoculated ear recurred sporadically during several months observation in about half the mice that survived intradermal infection with a selected type I isolate. The presence of virus in the ear tissue during such recurrences was confirmed by electron microscopy and isolation of infectious virus. The system of ear infection in the mouse is presented as a new model for studying neurovirulence, and latent and recurrent infection with herpes simplex virus.

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SUMMARYMild trauma was induced in the skin of mice latently infected with herpes simplex virus type I by stripping the originally infected ear with cellophane tape. Recurrent herpes simplex developed at this site 2 to 5 days later. It was detected clinically by the development of erythema and vesicles and by the appearance of virus in the skin. On any one occasion about 30 % of mice showed reactivated disease and increasing the severity of trauma did not increase this proportion. However the majority of animals developed reactivated disease on some occasions when stripping was repeated at monthly intervals. The results are discussed in relation to the skin trigger theory of reactivation of herpes simplex.

SUMMARYZosteriform spread of herpes simplex virus (HSV) infection occurs after primary inoculation of the skin of both outbred and inbred mice. With HSV type I strain SC 16 few outbred animals died if they were inoculated when 8 weeks old whereas up to 50 of animals died if inoculated when 4 weeks old. However, at either age, zosteriform spread of infection occurred in almost all animals as it did when 4-week-old outbred animals were inoculated with the avirulent strain KOS. Thus, control of zosteriform spread must act by different mechanisms from those controlling the encephalitis which leads to death. During replication in the epidermis virus enters axons and could first be found in sensory ganglia 2 days after inoculation of the skin. Thereafter, it was found in the nerve roots and in skin within the same dermatome but remote from the site of inoculation. When sensory nerves to this latter area were cut during the 4 days after primary inoculation lesions developing as a result of zosteriform spread were either completely inhibited or, with later section, decreased in incidence. Mortality was not affected by such nerve section. Latent infection must be established in neurons serving areas of skin remote from the inoculation site since with HSV-1 strain SC16, recrudescent lesions on the pinna could be induced by stripping the skin of the ear when the original inoculation had been in the skin of the neck. Such recrudescent disease was not demonstrated in animals infected with HSV-1 strain KOS even though this virus efficiently established latent infection in sensory ganglia.