Human CMV is one of the largest virus infecting human beings, belonging to the family of herpesviruses which are capable of persisting all lifelong in the infected cells alternating latency with reactivations.

Since CMV is capable of infecting the fetus following both primary and recurrent infection in immunocompetent women, and because the virus may be spread for years from infected children, CMV is the most common cause of congenital infections in developed countries.

Moreover, CMV is the most serious congenital infection being associated with severe neurological and sensorineural sequelae. Congenital CMV infection occurs in approximately 40% of infants born to mothers with primary infection. However, the transmission rates are about 30–40% in the first trimester, 35–55% in the second and 50–75%, in the third. The highest risk of severe sequelae (up to 50%) concerns a primary maternal infection occurring during the first 4 months of pregnancy because of the vulnerability of the embryonal cells to CMV replication and the lack of maternal and fetal immune defenses against the virus.

At birth, infected infants born to women with primary infection may have transient manifestations such as small for gestational age, jaundice, purpura, and hepatosplenomegaly, and/or severe damages including sensorineural hearing loss, and a neurological syndrome varying from seizures and abnormal muscular tone to microcephaly, periventricular calcifications, cerebral and cerebellar atrophy or malformations (polymicrogyria, lissencecephaly, etc.) These manifestations occur at rates ranging from 10% to 40%, depending on the time of maternal fetal CMV transmission.

Congenital infection can occur after recurrent maternal infection at an average rate of 1%, although higher rates have been reported. The infected infants are asymptomatic in the majority of the cases, and less than 10% of them have long-term sequelae including hearing loss psychomotor retardation, and cerebral palsy. However, the true frequency of affected infants may be higher than observed, since the presence of maternal antibody blunts the severity of fetal infection which could be associated with an early miscarriage or even a severely damaged embryo development.