Abstract
Objective: Mother-to-child transmission of the human immunodeficiency virus may be reduced with elective cesarean delivery before labor. Because immune activation enhances the human immunodeficiency virus infection, we hypothesized that fetal lymphocytes that are obtained at elective cesarean delivery may be less activated, therefore less susceptible to human immunodeficiency virus infection than cells that are obtained after normal spontaneous vaginal delivery at term. A second hypothesis was that intrapartum infection correlates with increased lymphocyte activation and susceptibility to human immunodeficiency virus infection. Study Design: Samples were obtained after normal spontaneous vaginal delivery (n = 13), elective cesarean delivery (n = 12), chorioamnionitis (n = 5), and preterm labor (n = 6). Activation markers were measured by flow cytometry, and cord blood mononuclear cells were infected with the human immunodeficiency virus. Results: Cell activation was comparable within the normal spontaneous vaginal delivery and elective cesarean delivery groups; there was no difference in susceptibility to in vitro human immunodeficiency virus infection. Intrapartum infection (chorioamnionitis, preterm labor) was associated with increased cell activation. Chorioamnionitis/preterm labor also tended to increase cord blood mononuclear cell susceptibility to human immunodeficiency virus infection. Conclusion: Labor did not activate fetal lymphocytes or alter susceptibility to human immunodeficiency virus infection compared with elective cesarean delivery. Intrapartum infection was associated with cell activation, and there was a trend toward increased susceptibility to human immunodeficiency virus infection. These data suggest that fetal lymphocyte activation correlates with susceptibility to human immunodeficiency virus infection and may account for the increased mother-to-child transmission of the human immunodeficiency virus that has been seen in association with chorioamnionitis and preterm labor. (Am J Obstet Gynecol 2002;187:1283-9.)
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