HIV-exposed uninfected (HEU) individuals are predisposed to adverse health outcomes, which in part may stem from the influence of an altered intrauterine milieu on fetal programming. The placenta serves as a readout for the effects of the maternal environment on the developing fetus and may itself contribute to the pathogenesis of disease.
U.S. academic health system.
We leveraged a previously established registry-based cohort of HEU adolescents and young adults to identify 26 subjects for whom placental histopathology was available. We further obtained placental tissue from 29 HIV-unexposed pregnancies for comparison. We examined differences in placental histopathology between groups, and related villous vascularity in the HEU group to prenatal maternal characteristics and long-term health outcomes.
Placentas from HEU pregnancies demonstrated a higher blood vessel count per villus as compared to controls (5.9 ± 1.0 vs. 5.4 ± 0.8, P = 0.05), which was independent of maternal prenatal age, race, BMI, smoking status, hemoglobin, and gestational age. Furthermore, within the HEU group, lower CD4+ T cell count during pregnancy was associated with greater placental vascularity (r = -0.44, P = 0.03). No significant relationships were observed between placental blood vessel count per villus and BMI z-score or reactive airway disease among HEU individuals later in life.
Placentas from HEU pregnancies demonstrated increased villous vascularity compared to HIV-unexposed controls in proportion to the severity of maternal immune dysfunction. Further studies are needed to examine intrauterine exposure to hypoxia as a potential mechanism of fetal programming in HIV.

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