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Cytomegalovirus (CMV) is one of the family of eight human herpesviruses,
designated as human herpesvirus type 5 (HHV-5) (Table
309-1). Taxonomically, it is referred to as a betaherpesvirus,
based on its propensity to infect mononuclear cells and lymphocytes
and on its molecular phylogenetic relationship to human herpesvirus
type 6 (HHV-6) and human herpesvirus type 7 (HHV-7). The virus consists
of a double-stranded DNA genome of > 240 kbp. The pathogenesis of
CMV infection has more recently been the subject of a comprehensive
review.4 As with the other herpesviruses, the structure
of the viral particle is that of an icosahedral DNA-contained capsid,
surrounded by a lipid bilayer outer envelope that
contains the virally encoded glycoproteins, which are the major
targets of host neutralizing antibody responses. The proteinaceous
layer between the envelope and the inner capsid, the viral tegument,
contains proteins that are targets of host cell-mediated immune
responses.
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Although most adults eventually become infected with cytomegalovirus
(CMV), the epidemiology of this infection is complex, and the age
at which an individual acquires CMV depends greatly on geographic
location, socioeconomic status, cultural factors, and child-rearing
practices.5-7 In developing countries, most children
acquire CMV infection early in life, whereas in developed countries,
the seroprevalence of CMV may be well below 50% in young
adults of middle-upper socioeconomic status.
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Transmission of CMV infection may occur throughout life, chiefly
via contact with infected secretions. CMV infections in newborns
are common, and most are subclinical. Approximately 1% (range
0.5–2.5%) of all newborns are congenitally infected
with CMV. Most infections occur in infants born to mothers with
preexisting immunity, and although clinically silent at birth, infection
can lead to long-term sequelae, most notably, sensorineural hearing
loss (SNHL).8 Additional information about congenital
CMV infection is presented in Chapter 231.
The route of acquisition of CMV infection acquired in utero is believed
to be transplacental.9 CMV may also be transmitted
perinatally, both by aspiration of cervicovaginal secretions in
the birth canal and by breast-feeding.10 Toddlers
are at high risk to acquire infection in daycare centers and may
in turn transmit infection to their parents.11-13 In
adults, sexual activity is a common mode of transmission.14 Although generally
asymptomatic, heterophile-negative mononucleosis can be a presentation
of primary infection in adulthood, as described later in this chapter.15 Blood
transfusion-associated CMV was once an important cause of morbidity
and mortality, notably in premature infants, but the routine use
of leukofiltration has largely eliminated the problem of posttransfusion
CMV.16
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In clinical specimens, one of the classic hallmarks of cytomegalovirus
(CMV) infection is the cytomegalic inclusion cell.
These massively enlarged cells (the property of “cytomegaly” from
which CMV acquires its name) contain intranuclear inclusions that
histopathologically have the appearance of “owl’s eyes” (Fig. 310-1). The presence of
these cells indicates productive infection in vivo, chiefly in ...