Mother-to-child transmission of GB virus C in a cohort of women coinfected with GB virus C and HIV in Bangkok, Thailand.

BACKGROUND: GB virus C (GBV-C) is an apathogenic virus that inhibits human immunodeficiency virus (HIV) replication in vitro. Mother-to-child transmission (MTCT) of GBV-C has been observed in multiple small studies. Our study examined the rate and correlates of MTCT of GBV-C in a large cohort of GBV-C-HIV-coinfected pregnant women in Thailand. METHODS: Maternal delivery plasma specimens from 245 GBV-C-HIV-infected women and specimens from their infants at 4 or 6 months of age were tested for GBV-C RNA. Associations with MTCT of GBV-C were examined using logistic regression. RESULTS: One hundred one (41%) of 245 infants acquired GBV-C infection. MTCT of GBV-C was independently associated with maternal antiretroviral therapy (adjusted odds ratio [AOR], 5.21 [95% confidence interval {CI}, 2.12-12.81]), infant HIV infection (AOR, 0.05 [95% CI, 0.01-0.26]), maternal GBV-C load (8.0 log(10) copies/mL: AOR, 86.77 [95% CI, 15.27-481.70]; 7.0-7.9 log(10) copies/mL: AOR, 45.62 [95% CI, 8.41-247.51]; 5.0-6.9 log(10) copies/mL: AOR, 9.07 [95% CI, 1.85-44.33]: reference, <5 log(10) viral copies/mL), and caesarean delivery (AOR, 0.26 [95% CI, 0.12-0.59]). CONCLUSIONS: Associations with maternal GBV-C load and mode of delivery suggest transmission during pregnancy and delivery. Despite mode of delivery being a common risk factor for virus transmission, GBV-C and HIV were rarely cotransmitted. The mechanisms by which maternal receipt of antiretroviral therapy might increase MTCT of GBV-C are unknown.

Placental abnormalities associated with human immunodeficiency virus type 1 infection and perinatal transmission in Bangkok, Thailand.

The effects of human immunodeficiency virus (HIV) type 1 on the placenta and the role of the placenta in mother-to-child HIV-1 transmission are not well understood. Placentas from 78 HIV-infected and 158 HIV-uninfected women were examined as part of a prospective perinatal HIV transmission study in Bangkok. HIV-infected women were more likely than HIV-uninfected women to have chorioamnionitis (odds ratio [OR], 2.1; P=.03), placental membrane inflammation (PMI; OR, 2. 7; P=.02), and deciduitis (OR, 2.3; P=.03) and less likely to have villitis (OR, 0.3; P=.02). However, among HIV-infected women, fewer women who transmitted infection to their child had chorioamnionitis (relative risk [RR], 0.2; P=.03), funisitis (RR, 0.4; P=.1), or PMI (RR undefined; P=.03). These findings suggest that, in this population, HIV-infected women are at increased risk for placental membrane inflammatory lesions, but that placental inflammatory lesions are not associated with increased perinatal HIV transmission.