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Human Cytomegalovirus (HCMV) is the most common cause of congenital infection in newborns. One mechanism for this virus to reach the fetus is to cross the placenta through the syncytiotrophoblast layer. Accumulation and protection of pathogens in the syncytiotrophoblast could affect the systemic distribution of pathogens and prolong maternal infections leading to increased incidence of fetal infections. Primary infections, reactivation or reinfection with another strain during pregnancy are risk factors for intrauterine HCMV transmission to the fetus. All lead to an active infection; however, viral load in blood or urine does not correlate with intrauterine transmission. I have shown that HCMV reversibly binds to the syncytiotrophoblast in vitro, protecting it from degradation. Furthermore, I demonstrated in vivo that HCMV is present in the placenta, even when cleared from maternal blood and urine. This evidence suggests increased potential for fetal transmission by virtue of continued virus localized at the maternal-fetal interface.