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Herpes simplex virus type 1 (HSV-1)
and herpes simplex virus type 2 (HSV-2) belong to a family of DNA
viruses that include cytomegalovirus (CMV), varicella-zoster virus
(VZV), Epstein-Barr virus (EBV), and human herpesviruses 6, 7, and
8 (Table 309-1). Following primary infection,
herpes simplex viruses establish a latent state, in general, HSV-1
in the trigeminal ganglion and HSV-2 in the sacral ganglion. From
time to time, the viruses may be reactivated, resulting in recurrent
infections that may or may not be associated with symptoms. HSV-1
is usually transmitted in oral secretions, whereas HSV-2 is most
often transmitted through sexual activity. HSV-1 infections occur
most frequently during childhood and usually affect body sites above
the waist (mouth, lips, eyes, face). HSV-2 infections occur most
often during adolescence and adulthood, and involve body sites below
the waist (genitalia, buttocks, thighs). Historically, the majority
of infections in newborns is transmitted from the maternal genital
tract and is usually caused by HSV-2.1 However,
because the prevalence of genital infection with HSV-1 in the United
States is increasing, a greater proportion of neonatal infections
may be due to HSV-1.2,3
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Humans are the only natural reservoirs of herpes simplex virus
(HSV). Infections caused by HSV have no seasonal predilection; however, geographic
location, socioeconomic status, age, and race influence the prevalence
of infection. Children of lower socioeconomic classes and those
from developing countries contract HSV-1 earlier in life than children
of more affluent socioeconomic classes and children from developed
countries. Increased direct person-to-person contact occurring in crowded
living conditions probably accounts for these differences.
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Primary infection with herpes simplex virus type 1 (HSV-1) usually
occurs in infancy or childhood, whereas primary infection with herpes
simplex virus type 2 (HSV-2) occurs after the onset ...