Abstract

Studies with human volunteers and patients suffering from recurrent herpes simplex virus (HSV) infections have shown that reinfections with autologous or heterologous strains, occurring at sites distant from those of the recurrences, are possible in a variable proportion of the subjects 1–5. Experiments in animals have shown that mice surviving a primary HSV infection in the lumbo-sacral area, can become latently infected in trigeminal ganglia upon reinfection of the orofacial site 6. Similar results were obtained after vaccination of mice with a thymidine-kinase negative, non-pathogenic HSV-1 mutant 7. It was also demonstrated that initial HSV-1 eye infection in rabbits prevents superinfection of trigeminal ganglia by other strains 8,9.

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