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  • • Most individuals with genital herpes are unaware of the infection but are able to transmit it to others.
  • • Type-specific serology allows reliable differentiation of chronic type 1 from type 2 infection.
  • • Clinical diagnosis should be confirmed by diagnostic testing of the genital lesion (culture or polymerase chain reaction [PCR]) or a type-specific serologic assay.

Herpes simplex virus (HSV) infections are endemic in the United States and are a cause of recurrent genital and oral ulcerative disease. Genital herpes infection can be caused by type 2 virus (HSV-2), or less frequently by type 1 (HSV-1). Although most infections are asymptomatic, genital HSV infection, whether type 1 or 2, can cause vesicular and ulcerative disease in adults and severe systemic disease in neonates and immunocompromised individuals. Genital HSV infection increases the risk of HIV acquisition in infected persons.

HSV-2 transmission is almost always sexual, whereas HSV-1 is usually transmitted through nonsexual skin-to-skin contact. Current estimates place the incidence of HSV-2 infection at more than 1.5 million cases annually. In the general population, HSV-2 seroprevalence is low for persons younger than 12 years of age, rises sharply following onset of sexual activity, and peaks by the early 40s. HSV-2 seroprevalence in the United States rose 30% between 1978 and 1991 to 21.7%. The overwhelming majority of individuals with genital HSV infection have undiagnosed initial infections and unrecognized recurrences. Orolabial HSV-2 infection is rare and is almost always associated with genital infection.

HSV-1 infection frequently occurs as orolabial infection in childhood, and approximately 20% of children younger than 5 years of age are seropositive. The seroprevalence of HSV-1 rises almost linearly with increasing age to approximately 70%. In the general population over the past decade, HSV-1 has become an increasingly common cause of genital infection, with an estimated 50% of newly acquired genital herpes attributable to it in some populations.

Fleming DT, McQuillan GM, Johnson RE, et al. Herpes simplex virus type 2 in the United States, 1976 to 1994. N Engl J Med 1997;337:1105–1111.  [PubMed: 9329932] (Classic article.)

Primary HSV infection occurs at mucosal sites of inoculation (see Figure 14–1), with retrograde infection propagating to sensory nerve ganglia. Following resolution of primary infection, HSV enters a latent state in sensory nerve ganglia from which reactivation may occur to cause active infection at any mucosal sites innervated by the nerve ganglia.

Figure 14–1.

Primary genital herpes of the vulva. (Reproduced, with permission, from Holmes KK, et al. Sexually Transmitted Diseases, 3rd ed. McGraw-Hill, 1999, Figure 28.)

During primary HSV infection, natural killer cells are important effectors of immunity. Their activation depends on the production of several cytokines in response to the infection. These cytokines also have direct and indirect effects that are important for limiting replication of the virus. As the immune response ...

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