Placental membrane inflammation and risks of maternal-to-child transmission of HIV-1 in Uganda

Prospective follow-up of 172 HIV-infected pregnant women and their infants was conducted at Mulago Hospital, Kampala, Uganda during 1990 to 1992. Info rmation was collected on maternal immune status (CD4 counts or clinical AID S), and concurrent infections with sexually transmitted diseases, Infants w ere observed on a follow-up basis to determine HIV infection, using polymer ase chain reaction (PCR) under 15 months of age and enzyme immunoassay/West ern blot for those older than 15 months. Placental membrane inflammation (c horioamnionitis and funisitis), and placental villous inflammation (villiti s, intervillitis, and deciduitis) were diagnosed by histopathology. Mother- to-child HIV transmission rates were assessed, and adjusted odds ratios (OR ) and 95% confidence intervals (95% CT) of transmission were estimated usin g women with no placental pathology or evidence of immune suppression as a reference group. Results: The overall mother-to-child HIV transmission rate was 23.3%. Women with no placental membrane inflammation or immune suppression had a transm ission rate of 11.3%; compared with 25.5% in women with placental inflammat ion and no immunosuppression (adjusted OR: 2.87; 95% CI, 1.04-7.90), and 37 .0% in immunosuppressed women (OR, 3.07; 95% CI, 1.42-6.67). We estimate th at 34% of HIV transmission could be prevented by treatment of placental mem brane inflammation in nonimmunocompromised women. Transmission rates were 4 0.9% with genital ulcer disease (OR, 3.57; 95% CI, 1.28-9.66). Placental vi llous: inflammation and artificial rupture of membranes did not increase tr ansmission rates and cesarean section was associated with a nonsignificant reduction of risk (OR, 0.70; 95% CI 0.24-2.06). Conclusion: Placental membrane inflammation increases the rate of mother-to -child HIV transmission.