Risk for perinatal HIV-1 transmission according to maternal immunologic virologic and placental factors.

1993 
Objective. —To evaluate how maternal and obstetric factors interact to influence mother-to-child human immunodeficiency virus type 1 (HIV-1) transmission. Design. —Prospective, observational cohort study of children born to HIV-infected women to determine child's HIV infection status. The analysis then compared peripartum maternal, placental, and obstetric variables between HIV-1 transmitter and nontransmitter women. Setting. —Two large maternity wards in Kinshasa, Zaire. Participants. —Consecutive sample of 324 HIV-1—infected women at delivery, with 254 HIV-seronegative women followed up as control subjects. Principal Outcome Measures. —HIV infection status of children, to classify each woman as an HIV-1 transmitter or nontransmitter. Results. —The highest transmission risk (TR) was associated with maternal p24 antigenemia (TR, 71%; relative risk [RR], 3.0; 95% confidence interval [CI], 1.7 to 5.2) and maternal CD8 + lymphocyte counts of at least 1.80×10 9 /L (1800/μL) (TR, 50%; RR, 2.2; 95% CI, 1.2 to 4.2). Among women with CD8 + lymphocyte counts of less than 1.80×10 9 /L, CD4 + lymphocyte counts of less than 0.60×10 9 /L were a risk factor (TR, 29%; RR, 2.2; 95% CI, 1.2 to 4.2). In women with neither high CD8 + nor low CD4 + lymphocyte counts, placental membrane inflammation was associated with perinatal transmission (TR, 40%; RR, 4.2; 95% CI, 1.3 to 13.7). In women with neither p24 antigenemia, high CD8 + or low CD4 + lymphocyte counts, nor placental membrane inflammation, the transmission risk was only 7%. Additional correlates of transmission included maternal anemia and fever, but not maternal sexually transmitted diseases. Conclusions. —Identifiable subgroups of HIV-1—infected women based on maternal and placental characteristics had between a 7% and 71% risk of perinatal HIV-1 transmission. Not only the overall rate of transmission but the impact of different risk factors for transmission appear to vary over the course of HIV infection. ( JAMA . 1993;269:2853-2859)
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