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I. DEFINITION

Human cytomegalovirus (CMV), also known as human herpesvirus 5, is a DNA virus and a member of the herpesvirus family (Herpesviridae).

II. INCIDENCE

CMV is the most common cause of congenital infection in the United States and occurs in approximately 0.5% to 1.3% of all live births. This results in approximately 40,000 new cases in the United States per year.

III. PATHOPHYSIOLOGY

CMV is highly species specific, and only human CMV has been shown to infect humans and cause disease. CMV is a ubiquitous virus that is transmitted in secretions, including saliva, tears, semen, urine, cervical secretions, blood (white blood cells), and breast milk. The seroprevalence increases with age and is influenced by many factors, such as hygienic circumstances, socioeconomic factors, breast feeding, and sexual contacts. In addition to transplacental infection, CMV may also be transmitted to the infant intrapartum (through exposure to CMV in cervical secretions), via breast milk, and via blood transfusion. CMV infection acquired during delivery or via breast milk is often asymptomatic in full-term infants with no effect on future neurodevelopmental outcome; however, a sepsis-like illness has been described in premature infants.

In developed countries, CMV seroprevalence varies inversely with socioeconomic status, with 40% to 80% of women of childbearing age in the United States having serologic evidence of past CMV infection. Seroconversion and initial infection can occur around the time of puberty, and shedding of the virus may continue for a long time. CMV can also become latent in white blood cells and reactivate periodically. In addition, a seropositive individual can be infected by a different strain of CMV. Reactivation and reinfection are grouped as a “nonprimary” infection.

CMV is capable of penetrating the placental barrier as well as the blood–brain barrier. During early pregnancy, CMV has a teratogenic potential in the fetus. CMV infections may result in neuronal migration disturbances in the brain. Both primary and nonprimary maternal CMV infection can lead to transmission of the virus to the fetus. When primary maternal infection occurs during pregnancy, the virus is transmitted to the fetus in approximately 35% of cases. The rate of fetal transmission appears to increase with advancing gestation; however, infection in early pregnancy causes more severe fetal infection with significant central nervous system (CNS) sequelae compared to infection acquired later. During nonprimary infection, transmission rate is low (only 0.2% to 1.8%), except for human immunodeficiency virus (HIV)-infected women, who show higher transmission despite receiving antiretroviral prophylaxis. Even though the risk for congenital infection is high after primary maternal infection, nonprimary infection is responsible for 75% of the overall burden of congenital CMV disease.

More than 85% of infants born with congenital CMV have a subclinical infection. Symptomatic infants are usually born to women with a primary infection. When the placenta becomes infected with CMV after a primary ...

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