156
Cytomegalovirus and Varicella–zoster Virus Vaccines
United States, there were approximately
4 million cases of varicella each year in
children, 11 000 hospitalizations, and 100
deaths each year, with half of the deaths in
children and half in adults infected for the
Frst time with VZV.
Passive immunization with high-titer
human antibody against VZV, known as
varicella-zoster immune globulin (VZIG),
and antiviral therapy with acyclovir, an
antiviral drug that inhibits the viral DNA
polymerase, can prevent or signiFcantly
reduce disease if administered within a
few days after exposure to VZV.
The same virus also causes the disease
knownasshinglesorherpeszoster,which
is most common in the elderly. This dis-
ease results from reactivation of the virus
that has been latent in sensory ganglia for
decades, with the skin lesions and accom-
panying pain usually localized to an area
of skin innervated by a speciFc sensory
ganglion. The major complication of her-
pes zoster is the ‘‘postherpetic neuralgia’’,
which may persist for months in elderly
patients. SpeciFc antiviral chemotherapy
or passive immunization with VZIG is
much less effective in treating reactivated,
secondary VZV infection compared to pri-
mary infection and varicella.
In contrast to chickenpox/varicella in
nonvaccinated children, most
primary
CMV infections of children or young
adults are mild or inapparent, with a
mononucleosis-like syndrome being one
of the more common symptomatic out-
comes in healthy young adults. Past infec-
tion with CMV, whether asymptomatic or
symptomatic, is indicated by the individ-
ual’s seropositivity in a laboratory assay for
anti-CMV antibody. The site of viral latency
following primary CMV infection is not as
well characterized as for VZV, but presum-
ably involves white blood cells known as
monocytes and polymorphonuclear leuko-
cytes. Serious infections are limited to
two major groups: infants infected during
pregnancy when virus from the infected
mother crosses the placental and infection
or reactivation in immunocompromised
persons such as immunosuppressed trans-
plant recipients or persons with AIDS.
An estimated 1% of all newborns have
congenital CMV, but less than 1/10th of
these CMV-infected newborns have seri-
ous, symptomatic infection at birth. Up
to 15% of the congenital infections that
are asymptomatic at birth may have later
neurological sequelae, especially hearing
defects. Intrauterine infection of the fe-
tus during the primary infection of the
mother, as compared to reinfection or reac-
tivation in the CMV-seropositive mother,
carries the highest risk of serious disease
and involves multiple organ systems. The
virus is commonly spread among children
in preschool and day-care centers because
the virus is shed in saliva and urine of
asymptomatic children, and it can also
spread to CMV-seronegative females of
childbearing age who work in these centers
or have a child in preschool or day care.
Similarly, the risk of serious and life-
threatening CMV disease in immunosup-
pressed recipients of kidney or liver trans-
plants is lower for seropositive persons un-
dergoing CMV reactivation or reinfection
versus seronegative persons acquiring pri-
mary CMV infection from the transplanted
organ. ±or CMV-seronegative patients who
will be receiving organ transplants from
CMV-seropositive donors, initiation of an-
tiviral therapy prior to the transplant can
reduce the severity of CMV infection trans-
mitted from the donor tissue. Reactivation
of CMV in seropositive patients under-
going bone marrow transplantation or in
patients with human immunodeFciency
virus and AIDS is also a signiFcant and
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