Maternal malaria and perinatal HIV transmission, western Kenya

Abstract

To determine whether maternal placental malaria is associated with an increased risk for perinatal mother-to-child HIV transmission (MTCT), we studied HIV-positive women in western Kenya. We enrolled 512 mother-infant pairs; 128 (25.0%) women had placental malaria, and 102 (19.9%) infants acquired HIV perinatally. Log10 HIV viral load and episiotomy or perineal tear were associated with increased perinatal HIV transmission, whereas low-density placental malaria (<10,000 parasites/mL) was associated with reduced risk (adjusted relative risk [ARR] 0.4). Among women dually infected with malaria and HIV, high-density placental malaria (>10,000 parasites/mL) was associated with increased risk for perinatal MTCT (ARR 2.0), compared to low-density malaria. The interaction between placental malaria and MTCT appears to be variable and complex: placental malaria that is controlled at low density may cause an increase in broad-based immune responses that protect against MTCT; uncontrolled, high-density malaria may simultaneously disrupt placental architecture and generate substantial antigen stimulus to HIV replication and increase risk for MTCT.

Figure 1

The effect of viral load and placental malaria density on risk for perinatal HIV transmission, western Kenya, 1996–2001. Women with low- (<10,000 parasites/μL, circles) and high- (>10,000 parasites/μL, squares) density placental malaria are compared with women without placental malaria (represented by the horizontal dashed line). RR, relative risk. Error bars refer to 95% confidence interval.

Figure 2

The effect of viral load and high-density placental malaria on risk for perinatal HIV transmission, western Kenya, 1996–2001. Women with high-density placental malaria (>10,000 parasites/μL) are compared to those with low-density placental malaria (<10,000 parasites/μL, represented by the horizontal dashed line). RR, relative risk. Error bars refer to 95% confidence interval.