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Placental Mitochondrial Dysfunction in relation to preterm delivery in HIV pregnancy

University of British Columbia

Background: Preterm birth (PTB) (<37 weeks of gestation), is the leading cause of mortality and morbidity among children, responsible for >1 million deaths in 2015 [1]. In North America, PTB occurs in 6–10% of births. However, among pregnant women living with HIV, the rates are higher (18-29%). To date, there is no generally accepted mechanism underlying such increased rates. One possible explanation is reduced maternal progesterone production during pregnancy, which may be related to HIV infection and/or antiretroviral (ARV) treatment. Synthesis of progesterone (hormone central to pregnancy maintenance), is dependent on placental mitochondrial function. Given that many ARVs can affect mitochondrial (mt) function, I investigated the possible effects of ARV on placental mtDNA content and progesterone levels. Methods: 136 HIV+ and 60 HIV- pregnant women were enrolled in the Canadian prospective study, the Children and women: Antiretroviral and Markers of Aging (CARMA) cohort. Placenta and blood specimens, as well as clinical and sociodemographic data, were collected. Placental and plasma progesterone levels, as well as placenta mtDNA content, were measured using ELISA and qPCR respectively. We extended these investigations of ARV effects to in vitro models on two human placental cell lines, JEG-3 and BeWo. Results: Within this cohort, HIV-exposed uninfected (HEU) infants were born at an earlier gestational age (p=0.017), with a lower birth weight (p=0.011) compared to controls. PTB showed no association with HIV status, placenta mtDNA or progesterone levels. However, higher mtDNA was associated with preeclampsia (p<0.001), which often leads to PTB.

Text

2018-01-17

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/64388

Pathology and Laboratory Medicine

University of British Columbia

UBCV

http://creativecommons.org/licenses/by-nc-nd/4.0/