# Placental Microvasculature in Pregnancies Complicated by HIV

> **NIH NIH R21** · GEORGETOWN UNIVERSITY · 2020 · $209,551

## Abstract

PROJECT SUMMARY
Disparate outcomes in HIV positive pregnancies, such as fetal growth restriction (FGR), are etiologically poorly
understood, but are attributed to uteroplacental insufficiency. FGR is a serious adverse outcome with
associated lasting morbidity for the HIV exposed infant. Further research is desperately needed to better
understand the placental pathophysiology in order to predict, diagnose, monitor, and potentially
prevent FGR. Our previous research demonstrated increased microvascular oxidative stress in reproductive
age women living with HIV (WLHIV) and alludes to a possible placental pathophysiology. Gluteal biopsies in
premenopausal WLHIV without overt cardiovascular risk factors revealed severe endothelial dysfunction and
reduced nitric oxide. These finding in non-pregnant WLHIV may represent early markers of future
cardiovascular morbidity and beg the question of possible systemic microvascular dysfunction, including in the
placenta. Although these findings in gluteal tissue cannot be directly extrapolated to placental
microvasculature, we hypothesize that there is of potential systemic effect of HIV infection or ART on
microvascular pathophysiology, similarly affecting the placenta, with a detrimental effect on fetal
growth. The limited literature on human placental microvessels, particularly studies of placentas with growth
restriction, yielded conflicting results largely attributable to methodological inconsistencies.
To further explore this hypothesis, we are proposing a pilot study to replicate the methodology used in gluteal
tissue in placental tissue and to characterize differences in placental microvascular nitric oxide (NO), reactive
oxygen species (ROS), contractility, and endothelial dysfunction in pregnancies complicated by HIV and
growth restriction. Addressing HIV-associated comorbidities and complications, specifically
cardiovascular, are stated priorities of the NIH Office of AIDS Research and better understanding the
underlying pathophysiology of the adverse outcomes related to pregnancies complicated by HIV have
critically important implications for WLHIV and their pregnancies. Specifically our aims are 1) To
determine the best methods of measuring contractility and endothelial function of microvessels in the
human placenta and to adapt laboratory methodologies previously employed to measure the same
parameters in gluteal tissue; 2) To undertake a quantitative evaluation of differences in microvascular NO,
ROS, contractility, and endothelial dysfunction in 12 placentas of pregnancies complicated by HIV with and
without FGR and 12 placentas of pregnancies in HIV-negative matched controls with and without FGR.
This pilot research is the crucial next step to better understanding, diagnosing and managing the
placental pathophysiology associated with adverse fetal and neonatal outcomes in pregnancies
complicated by HIV.

## Key facts

- **NIH application ID:** 9925912
- **Project number:** 1R21HD101340-01
- **Recipient organization:** GEORGETOWN UNIVERSITY
- **Principal Investigator:** Rachel K Scott
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $209,551
- **Award type:** 1
- **Project period:** 2020-08-01 → 2022-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9925912

## Citation

> US National Institutes of Health, RePORTER application 9925912, Placental Microvasculature in Pregnancies Complicated by HIV (1R21HD101340-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9925912. Licensed CC0.

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