Congenital cytomegalovirus infection: impairment and immunization.

(See the articles by Ogawa et al., on pages 782–8, and by Schleiss et al., on pages 789–98.) It has been 50 years since Smith [1] and Weller et al. [2] separately reported the isolation and propagation of a cytopath-ogenic virus from tissues of infants with cytomegalic inclusion disease. In the intervening half century, much has been learned about congenital cytomegalovirus (CMV) infection, as well as the epidemiological , transmission, and molecular biological characteristics of CMV and the natural history of CMV infection. Unfortunately , no means of preventing congenital CMV infection or its cognitive, motor, or sensory sequelae is available or even on the visible horizon. In this issue of the Journal, Ogawa et al. [3] and Schleiss et al. [4] add to our knowledge of the role of congenital CMV infection in severe hearing loss and inform continuing investigation of vaccine approaches to prevention , respectively. The respective topics of these reports—hearing loss and vaccine prevention—also remind us that research on congenital CMV infection continues to be driven by the initiative of individual investigators. Ogawa et al. [3] took advantage of umbilical cord specimens, which are saved by families in Japan as a keepsake. They tested children with severe sensorineural hearing loss for congenital CMV infection and for the connexin 26 gene, GJB2, mutations in which are the leading genetic cause of hearing loss. Although knowledge about the sensitivity and specificity of the poly-merase chain reaction (PCR) assay used for the detection of human CMV (HCMV) glycoprotein H and the real-time PCR assay for UL83 is not extensive, the authors report that umbilical-cord samples from 4 children with known congenital CMV infection were all positive when both assays were used and that samples from 17 healthy children were all negative. Among children with severe hearing loss, 10 (15%) were positive for CMV by both PCR assays , and 16 (24%) were positive for mutations in GJB2. There was no overlap in the 2 groups; none of the children with congenital CMV infection had mutations in the connexin 26 gene. This study provides evidence that congenital CMV infection and GJB2 mutations account for roughly similar proportions of severe hearing loss in children in Japan and that the association between congenital CMV infection and hearing loss is not due to the coincident occurrence of CMV infection in children with GJB2 mutations. Review of the medical records of the children with …