摘要：

The epidemiology of herpes simplex virus (HSV) infections in man has a number of unusual features (see Whitley, this volume). In particular, the recurrent lesions (herpes labialis, herpes genitalis, and herpes keratitis) often appear at the same peripheral site, the recurrences are often precipitated by particular stimuli, e. g., fever, excess exposure to sunlight, etcetera, and serum antibodies to the virus remain constant throughout life irrespective of the frequency of recurrent disease. Moreover, during intervals of clinical normality it has proved difficult to isolate virus from peripheral tissues such as the skin where lesions are prone to occur (see Section II.B). Such observations led to the concept that recurrent herpetic disease arises from an endogenous, lifelong, "hidden" or latent infection rather than from frequent exogenous reinfection with the virus (Burnet and Williams, 1939). This "natural history" of the virus infection poses a number of fascinating questions: What tissue or tissues harbor the latent infection? How is the latent infection established and maintained? What mechanisms underlie the reactivation of latency and the production of recurrent disease? Such questions have intrigued virologists since the early part of this century but definitive answers only began to appear during the last decade. In particular, the experimental confirmation of the role of the nervous system in latent infections with HSV has prompted a number of recent excellent reviews (Stevens and Cook, 1973a,b; Docherty and Chopan, 1974; Baringer, 1975; Stevens, 1975, 1978, 1980; Klein, 1976; Longson, 1978; Wildy et al ., 1982).

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