All HIV-positive mothers received intrapartum ZDV. Infant characteristics are shown in Table 2. Groups were not statistically different with regard to sex and birth weight, but the HIV-exposed infants had a lower gestational age and birth weight compared with the control infants. All HIV-exposed infants received antiretroviral

prophylaxis, with the majority receiving ZDV monotherapy. No HIV-exposed infant had any clinical abnormalities consistent with mitochondrial disease. Subsequent HIV RNA/DNA results excluded HIV infection in all HIV-exposed infants. Mitochondrial and oxidative stress assessments for placenta, umbilical cord blood and peripheral infant blood are shown in Table 3. Placental mtDNA copies/cell was not statistically different between the HIV-infected group and the control Palbociclib mw group. Also, there was no difference between groups in MDA, a measure of oxidative stress. No correlation was found between the oxidative marker MDA and the mtDNA content. The mtDNA content was not statistically different between groups in the umbilical cord blood, but the mitochondrial find more enzyme expression level was significantly decreased in the HIV-exposed group. Figure 1a shows the distribution of COX II:IV values for HIV-positive subjects and controls. In contrast to the umbilical cord blood, the mtDNA content in the peripheral infant blood was significantly increased

in the HIV-exposed group compared with the controls. However, mitochondrial enzyme expression level was not statistically different between the groups. Figure 1b shows the distribution of mtDNA content for both groups. Two multivariable linear regressions were conducted in order to investigate the variables associated with [1: the decreased

mitochondrial enzyme expression Thiamet G level in the umbilical cord blood in the HIV-positive/HIV-exposed group, and [2: the increased mtDNA content in the HIV-exposed infants. In the first model, treatment group (HIV-positive/HIV-exposed vs. HIV-negative/HIV-unexposed) was the only significant variable associated with umbilical cord blood mitochondrial enzyme expression level (Table 4a). The umbilical cord blood COX II:IV ratio decreased by an average of 66.6 in the HIV-positive/HIV-exposed group than in the controls. In the second regression model, the only variables that were significant were treatment group (HIV/ART-exposed vs. HIV/ART-unexposed) and maternal age (Table 4b). Here, the mtDNA content in the infants was an average of 395 copies/cell higher in the HIV-exposed infants than in the controls. Also, the mtDNA content increased by an average of 59 copies/cell in the infant for every 10-year increase in the women's age. ART given to HIV-infected women during pregnancy and to their infants postnatally has drastically decreased the risk of MTCT of HIV [1]. In high-income countries, HIV-infected pregnant women receive a potent combination of antiretrovirals, including a backbone of two or more NRTIs.