BROGLY ET AL. RESPOND

We would like to thank Woo and Sterling1 for their suggestion of alternative or complementary modes of transmission for the genital condylomata that we observed in young girls enrolled in the Pediatric AIDS Clinical Trials Group protocol 219C who had been perinatally infected with human immunodeficiency virus.2 We speculated that these cases of genital condylomata might have occurred through perinatal transmission of the human papilloma virus (HPV), transmission of HPV through sexual activity, or through sexual abuse, the latter of which was identified as the likely cause of HPV infection in 31% of 55 children following a retrospective review of clinical data.3 We did not discuss the possibility of nonsexual, postnatal transmission of HPV as raised by Woo and Sterling. Indeed, close nonsexual contact and self-inoculation are possible modes of HPV transmission, and should have been included.

Unfortunately, HPV typing was not collected in protocol 219C, and we were unable to include these findings as discussed in our paper.2 However, we were able to correlate the presence of genital condylomata at a young age with the occurrence of abnormal cervical cytology during adolescence. A total of 4 of 23 girls with genital condylomata documented before 13 years of age had subsequent cervical Papanicolaou smears recorded in protocol 219C. All 4 of these girls had abnormal cervical cytology, 3 had low-grade squamous intraepithelial lesions, and 1 had abnormal cells of undetermined significance.

The multiple potential modes of HPV transmission and frequency of childhood genital condylomata cases documented in this and other studies3^,4 underscore the need for additional research in this area.