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Introduction ============ Human cytomegalovirus (CMV) is a ubiquitous beta-herpes virus that leads to congenital infection in 0.4% to 2.3% of all newborns.[@b1-ijwh-2-023] The risk of intrauterine transmission after primary CMV infection during pregnancy approaches 40%, with an increased risk of adverse fetal effects if infection occurs during the first half of pregnancy.[@b2-ijwh-2-023] Of congenitally infected infants, approximately 10% are symptomatic at birth. Of the remaining 90% of infants who are asymptomatic at birth, 10%--15% will subsequently manifest evidence of permanent sequelae.[@b3-ijwh-2-023] Congenital CMV is a significant cause of neurodevelopmental disability, including sensorineural hearing loss (SNHL) and intellectual disability (previously referred to as "mental retardation"). More children suffer from long-term sequelae as a result of congenital CMV infection than Down syndrome or fetal alcohol syndrome.[@b4-ijwh-2-023] In this review, current concepts regarding the epidemiology, pathogenesis, and prevention of CMV infection are summarized, with an emphasis on strategies designed to improve awareness of the risk of CMV among women of childbearing age. Epidemiology ============ CMV is found worldwide, with the rate of seropositivity affected by geographic, socioeconomic, and ethnic background.[@b2-ijwh-2-023],[@b3-ijwh-2-023] In developed countries, the prevalence of CMV seropositivity is 40% to 60% in individuals of middle to upper socioeconomic status and ∼80% among those of lower socioeconomic status.[@b3-ijwh-2-023] By comparison, virtually individuals in developing countries have been infected by CMV in early childhood.[@b3-ijwh-2-023] In the United States, the seroprevalence of CMV is higher among non-Hispanic blacks and Mexican Americans than among non-Hispanic whites.[@b5-ijwh-2-023] Congenital CMV infection can occur as the result of a primary CMV infection, reinfection with a new strain of CMV, or reactivation of a latent infection.[@b6-ijwh-2-023],[@b7-ijwh-2-023] Maternal immunity to CMV provides some protection against vertical transmission of the virus. If a primary CMV infection occurs in the period just prior to conception, the risk of transmission is 8.7%.[@b8-ijwh-2-023] Primary maternal CMV infection occurring in the first, second, and third trimester results in congenital infection in approximately 25%, 50%, and 75% of fetuses, respectively.[@b9-ijwh-2-023] In contrast, the risk of CMV transmission to the fetus after a recurrent maternal infection is only 0.15 to 2%.[@b10-ijwh-2-023],[@b11-ijwh-2-023] Fowler et al demonstrated a 69% reduction in the risk of congenital CMV infection in future pregnancies in women who were seropositive for CMV when compared to seronegative women.[@b12-ijwh-2-023] However, despite the risk reduction preconception immunity affords, over 60% of infants with congenital CMV infection are born to mothers with immunity to CMV prior to pregnancy, reflecting the high rate of CMV seropositivity in the population.[@b13-ijwh-2-023] In populations with high maternal CMV seropositivity, the incidence of congenital CMV infection is greater than in populations of lower maternal seroprevalence.[@b1-ijwh-2-023] It has generally been believed that the fetuses of pregnant women with preconception immunity to CMV are somewhat protected against the most significant neurodevelopmental sequelae of congenital CMV infection. A study comparing women with preconception immunity to CMV to those who acquired primary CMV infection in pregnancy showed that the women with preconception immunity have a significant reduction in transmission of CMV to the fetus, as well as decreased