Abstract
AbstractBackgroundPreterm birth is a significant global issue. Antiretroviral therapy (ART) use and human immunodeficiency virus (HIV) infection have both been linked in recent research as independent risk factors for preterm birth. Although there has been evidence linking preterm delivery to significant pathological alterations in the placenta, it is still unclear how exactly HIV and ART harm the placenta and raise the risk of prematurity. To explain the increased risk of preterm birth (PTB), we set out to describe the surface morphological alterations in placenta villi associated with HIV and ART.Methods and materialsWe collected and processed 160 placentas from 40 HIV-positive women on ART and 40 HIV-negative women who had preterm deliveries, 40 HIV-positive women and 40 HIV - negative women with term delivery in Nairobi, Kenya. The placenta biopsies were harvested, washed in phosphate buffer solution, and processed for scanning electron microscopy. The dried tissue was mounted onto specimen stubs, sputter coated with gold and visualized using Zeiss Merlin FESEM in-lens. Forty representative samples, 10 from each group, were randomly selected and examined by investigators who were blinded to maternal HIV serostatus.ResultsThe average gestational age for preterm and term births was 34 and 39 weeks, respectively. The average age of the mothers of preterm and term babies was 26.8 + 4.6 years and 24.3 + 4.3 years, respectively. The villous core of the placenta from HIV-negative patients was covered with microvilli that varied in size and appearance, and there were hardly any residual red blood cells. Placenta from HIV-positive women with preterm birth had widespread damage with shrunken and wrinkled villi, predominant blunting of the microvilli, with attendant syncytiotrophoblast disruption, and significant erythrocyte adhesion within extensive fibrillar meshwork and on surface of the syncytium.ConclusionOur results show distinctive alterations in the placenta of HIV-positive mothers who gave birth prematurely, which may impair the syncytium’s ability to function normally. Microvilli blunting, syncytial disruptions, and syncytial erythrocyte adhesion might be the symptoms of a deeper biological process. Further work to understand the effect of HIV/ART on the syncytiotrophoblast in relation to prematurity is recommended.
Publisher
Cold Spring Harbor Laboratory