Congenital CMV is the most common congenital infection in the developed world. Infection results in congenital disease ranging from asymptomatic infection to severe neurodevelopmental impairment, and occasionally fetal or neonatal death. Fetal infection can occur through maternal-fetal transmission during primary maternal infection or maternal reactivation or re-infection. Awareness among maternal health care providers and parents is low. The prevention of maternal CMV infection currently relies on hygiene measures, with no effective CMV vaccine or prophylactic therapies. No licensed treatment options are available to prevent maternal-fetal transmission or fetal disease. Hyperimmunoglobulin and valaciclovir have been investigated for prevention of maternal-fetal transmission or fetal treatment, with some evidence supporting consideration of maternal administration of hyperimmunoglobulin or valaciclovir therapy in certain circumstances. This article outlines the clinical evidence regarding proven preventative behavioral measures and experimental hyperimmunoglobulin and valaciclovir therapies, that is structured around common questions asked by pregnant women about CMV infection. It is aimed to help maternity health care providers counsel prospective parents about congenital CMV disease and the preventative and therapeutic strategies currently available. 1 | INTRODUCTION Congenital CMV infection remains a predominant infectious cause of lifelong disability, as well as a cause of stillbirth and neonatal mortality. It is estimated that 1 in 150 infants are born with congenital CMV infection, making it the commonest congenital infection in the developed world. 1,2 Congenital CMV can occur through primary infection in seronegative pregnant women or through CMV reactivation or re-infection in seropositive pregnant women. 3 However, the likelihood of maternal-fetal transmission of CMV is much higher for primary maternal infection (32%) compared with recurrent maternal infection (1.4%). 1 In addition, first trimester infection is also associated with increased rates of adverse neonatal/infant outcomes compared with infection later in pregnancy (20%-45% vs 6%-17%). 4 Overall, when a mother has primary CMV in the first trimester, it is estimated that 1 in 10 fetuses or neonates will have an adverse perinatal outcome. 4 This may involve sensorineural hearing loss (SNHL), chorioretinitis, microcephaly, hepatomegaly, jaundice, thrombocytopenia, neurodevelopmental impairment, stillbirth, or neonatal death. Of those with symptomatic congenital CMV at birth, approximately one in two infants will have permanent sequelae, chiefly SNHL or