Extract

(See the Major Article by Visentin et al, on pages 497–503.)

A primary maternal infection with cytomegalovirus (CMV) during early pregnancy accounts for the majority of congenital disease due to CMV. This is a major public health problem, and in the United States approximately 9000 children are born each year with severe disabilities caused by this placental and intrauterine infection [1]. Immunity induced by infection with wild-type CMV affords women a high degree of protection against acquisition of a second CMV infection and protects the fetuses from severe postnatal neurosensory deafness and neurologic damage. For women who are immune to CMV before conception, the intrauterine fetal infection rate is approximately 1%, and >90% of infants are healthy. For women who acquire CMV during pregnancy, the fetal infection rate varies from 33% to 75% as gestation progresses, and the disease rates may be as high as 50% if infection occurs during the first half of pregnancy [2, 3]. These observations suggest that an active CMV vaccine is feasible and that it has no theoretical or biological obstacles. Both active and passive immunization experiments have been successful in a guinea pig model of congenital infection [4–7]. There have been 2 human trials of active immunization whose end points were the prevention of maternal infection. One trial of a live attenuated vaccine, conducted in the early 1990s, failed because of poor antibody levels associated with a vaccine dose that was too low [8]. A second trial, reported in 2009, used a protein vaccine (gB/MF59). This vaccine was 50% effective in preventing maternal infection in nonpregnant women [9]. A third trial of gB/MF59 that involves a similar study design is ongoing.

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