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Early this century, the term cytomegalic inclusion disease (CID) was used to designate the cellular changes characterized by enlargement and typical intranuclear inclusions observed in tissues of fetuses and infants with a fatal illness. In 1957, Smith and Weller et al, identified the causative agent of CID, which was named cytomegalovirus (CMV) by Weller in 1960. By 1971, it was clear that congenital human CMV (HCMV) infection was an important health problem. Since then, many advances have been made in the diagnosis, therapy, and knowledge of the epidemiology of congenital HCMV infection. However, most of these improvements, particularly those concerning diagnostic technologies and development of antiviral drugs, have been the result of the powerful effort to reduce the devastating impact of HCMV infections in AIDS and transplanted patients. Indeed, it is disappointing to observe that in the year 2000 CID does still occur, that HCMV is still recognized as the leading cause of congenital infection and the leading infectious cause of mental retardation and deafness, and, most important, that no active prevention is available for seronegative women. Moreover, because of the limited possibilities of prophylaxis and treatment, and the misuse of the currently available serologic assays, the issue of whether the determination of HCMV antibody status for women of childbearing age is justified has become a matter of debate.