The problem of congenital HCMV infection is unquestionably the major driving force behind efforts to develop a HCMV vaccine. In the developed world, HCMV is the most common congenital viral infection (Whitley 1994). Estimates of the prevalence of congenital HCMV infection suggest that between 0.5% and 2% of all newborns in the developed world are infected in utero (Demmler 1996). In the United States alone, this corresponds to approximately 40,000 infected newborn infants born annually with HCMV infection. The concern is particularly acute for HCMV-seronegative women of child-bearing age. Based on recent HCMV incidence estimates, approximately 27,000 new infections are believed to occur among seronegative pregnant women in the United States each year (Colugnati et al. 2007). Approximately 10% of congenitally infected infants have clinically evident disease in the newborn period, including visceral organomegaly, microcephaly with intracranial calcifications, chorioretinitis, and skin lesions including petechiae and purpura. Although the majority of congeni-tally infected infants appear normal at birth, these children are nonetheless at risk for neurodevelopmental sequelae, in particular sensorineural hearing loss (SNHL). Antiviral therapy in infected newborns with neurologic involvement is of value in ameliorating the severity and progression of SNHL (Kimberlin et al. 2003), but the toxicities of available antiviral agents are of concern, and the benefits of therapy are limited. Therefore, there are few medical interventions currently available to prevent or limit HCMV-induced neurological morbidity in infants, underscoring the urgent need for vaccine development.
Was this article helpful?