The natural history of CMV infection during pregnancy is complex and has not been defined completely. A schematic representation of the consequences of CMV infections during pregnancy is shown in Fig. 1. Unlike rubella and toxoplasmosis, for which intrauterine transmission occurs only as a result of primary infection acquired during pregnancy, congenital CMV infection has been shown to occur in children born to mothers who have had CMV infection prior to pregnancy (nonprimary infection) (16,49-51). In fact, congenital CMV infection following a nonprimary maternal infection has been shown to be common, especially in highly immune populations (7,16,49,51).
Although the pathogenesis of intrauterine transmission of CMV has not been clearly defined, maternal immune response has been shown to be a crucial determinant of the transplacental transmission of CMV. The importance of maternal immune responses is evident by the substantial protection that preconceptional immunity to CMV provides against intrauterine transmission and damaging fetal infection. Although this protection is not complete, the transmission rates decrease by about 25-fold in mothers with preconceptional immunity compared to those with primary infection (17,20,52). Primary maternal infection is defined as an initial acquisition of CMV during pregnancy and is identified by conversion from serum antibody-negative to antibody-positive status or by the detection of circulating immunoglobulin (Ig) M antibody to CMV. However, one should be cautious with this definition because the presence of CMV IgM antibodies against CMV has been demonstrated in women with evidence of past infec-
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