Abstract

The two types of herpes simplex virus—HSV-1 and HS V-2—are morphologically indistinguishable and consist of 150-mm particles with a DNA-containing core that is enclosed in an envelope. The two virus types can be distinguished by biologic, biochemical, and antigenic properties; however, the typical clinical lesions associated with infections by the two viruses are very similar. Generally, HSV-1 has been isolated from oral-facial lesions, as well as from cases of herpetic keratoconjunctivitis and encephalitis, while HSV-2 has been recovered from genital lesions, infants with neonatal systemic herpes, and cases of herpetic meningitis. 1 These associations of virus types with clinical diseases are not absolute. HSV-1 or HSV-2 may produce a number of clinically distinguishable illnesses. Each of these illnesses has certain epidemic-logic features that are unique. For example, Kaposi's varicelliform eruption represents a generalized cutaneous infection occurring primarily among persons suffering from atopic eczema 2–4 or Darier's disease. 5 Herpetic whitlow occurs commonly among physicians, dentists, and nurses who occupations require manual contact with individuals who may be shedding virus. 6–8 A form of cutaneous herpes has been described among wrestlers and has been called herpes gladiatorium. 9,10 Anorectal herpes has been reported with increasing frequency, and the majority of cases reported have occurred in homosexual men. 11,12 Aseptic meningitis is an occasional complication of genital herpetic infections and occurs mostly in young adults. 13–15 The vast majority of illness, however, results from infections initiated in the oral cavity or the genital tract, and these will be considered in more detail. Our knowledge of the epidemiology of HSV-1 and HSV-2 comes from studies that have varied considerably in design and in the populations examined. The epidemiology of clinical illnesses has been delineated primarily by periodically examining patients in described populations or from questionnaire surveys. Information about the occurrence of infections, many of which are asymptomatic, has come from serologic surveys or from surveys of virus shedding. Each method has limitations and the conclusions drawn from these different approaches have not always been similar. In this review, the conclusions drawn are those that are most consistent with the data available.

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