Introduction

Cytomegaloviruses (CMV) were initially identified by distinct histopathological findings that were observed in tissue from a variety of infected mammals, including humans. Perhaps the most well-recognized finding were inclusion bearing cells in the salivary glands of infected animals (Jesionek and Kiolemenoglou, 1904; Ribbert, 1904; Goodpasture and Talbot, 1921; Cole and Kuttner, 1926). Similar histopathologic findings of intracellular inclusions were noted in tissues from infants dying as a result of severe congenital (present at birth) cytomegalovirus infection leading to the designation of this clinical syndrome as cytomegalic inclusion disease (Farber and Wolbach, 1932). Studies by several groups of investigators provided compelling evidence from natural history studies that HCMV was a relatively frequent cause of disease in infants infected in utero and, that this viral infection could result in neurologic impairment in infected infants (Hanshaw, 1971; Stagno et al., 1977; Pass et al., 1980; Williamson et al., 1982; Bale, 1984; Fowler et al., 1992). Importantly, these early studies demonstrated that even infants with subclinical or silent infections could develop neurological sequelae (Stagno et al., 1982, 1983; Williamson et al., 1992). In the late 1960s, HCMV was recognized as a significant cause of disease in allograft recipients and in the case of hematopoietic allograft recipients, HCMV infection became recognized as one of the most frequent causes of death in the post-transplant period (Rifkind, 1965; Myers et al., 1975; Ho, 1977; Rubin et al., 1979; Winston et al., 1979; Rubin et al., 1981; Rubin and Colvin, 1986; Rubin, 1990).