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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.




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.


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




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 ...

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