- • 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
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.
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 ...