Abstract 919 Poster Session IV, Tuesday, 5/4 (poster 146)

Congenital CMV infection is the leading cause of brain damage and hearing loss in children. To determine whether the virus burden in early infancy predicts the long-term outcome, urine CMV titers and CMV DNA in peripheral blood leukocytes (PBL) were quantitated in 80 infants (61 asymptomatic and 19 symptomatic) with congenital CMV infection born between 1994 and 1997. Urine and PBL samples were obtained at the initial visit within the first 2 months of life. CMV viruria was titered in 73 children, and PBL samples from 60 infected children were initially tested for the presence of CMV DNA by PCR with the positive samples quantitated for the amount of viral DNA. PCR primers were selected to amplify a 298 bp target sequence from the highly conserved AD-1 region of glycoprotein B (gB) of CMV. A quantitative-competitive PCR in which a competitor plasmid contained the target sequence of gB but had a 77 bp deletion in the center of the sequence was used to measure viral load, and the results were expressed as copies of viral genome/ml of blood. The study children were followed longitudinally in a special clinic to assess outcome. At least one sequela was observed in 7/61 (11%) asymptomatic and 11/19 (58%) symptomatic infants. PCR was positive in 11/16 symptomatic and 21/44 asymptomatic children, and the presence of CMV DNA in peripheral blood did not correlate with the development of sequelae. Quantitation of CMV viruria showed a significantly higher urine titer in 16/73 children with at least one sequelae compared to 57 children without sequela (mean titer 2.7 × 105 vs 4.8 × 104, p<.005). Among the 31 children in which CMV viral load was quantitated, the group of 7 children with at least one sequela had higher virus burden than those with no sequelae (p<.05). However, only 2/20 children in whom viral load could be estimated developed sequelae. The results of this study demonstrate that in children with congenital CMV infection, those with symptomatic infection and with sequelae on follow-up, exhibited an increased virus burden. These results suggest that measurement of virus burden in the newborn period by quantitating CMV viruria and viral DNA in peripheral blood could prove useful as a predictor of long-term outcome in children with congenital CMV infection. However, the association of viral load and outcome in children with asymptomatic infection remains to be defined.