Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 224, Issue -, Pages S694-S700Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiab201
Keywords
Malperfusion; small for gestational age; intra- uterine growth restriction; Africa; resource-limited; pregnancy; pregnant; immunohistochemistry; histology; pathology
Categories
Funding
- Harvard University Center for AIDS Research, National Institutes of Health [P30AI060354]
- National Institute of Allergy and Infectious Diseases, National Institutes of Health [P30AI060354]
- Harvard Catalyst, the Harvard Clinical and Translational Science Center (KL2/Catalyst Medical Research Investigator Training award [KL2TR002542]
- Charles H. Hood Foundation
- National Institute of Allergy and Infectious Diseases [K23AI138856, K24AI141036]
- American Society of Tropical Medicine and Hygiene (Burroughs Wellcome Fellowship)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development [K23HD097300]
- Massachusetts General Hospital Executive Committee on Research through the Center for Diversity and Inclusion
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Women with HIV are at higher risk of adverse birth outcomes, possibly due to placental vasculopathy, but further research is needed to confirm this.
Background. Women with human immunodeficiency virus (HIV) (WHIV) are at higher risk of adverse birth outcomes. Proposed mechanisms for the increased risk include placental arteriopathy (vasculopathy) and maternal vascular malperfusion (MVM) due to antiretroviral therapy and medical comorbid conditions. However, these features and their underlying pathophysiologic mechanisms have not been well characterized in WHIV. Methods. We performed gross and histologic examination and immunohistochemistry staining for vascular endothelial growth factor A (VEGF-A), a key angiogenic factor, on placentas from women with >= 1 MVM risk factors including: weight below the fifth percentile, histologic infarct or distal villous hypoplasia, nevirapine-based antiretroviral therapy, hypertension, and preeclampsia/ eclampsia during pregnancy. We compared pathologic characteristics by maternal IIIV serostatus. Results. Twenty-seven of 41 (placentas 66%) assessed for VEGF-A were from WHIV. Mean maternal age was 27 years. Among WHIV, median CD4 T-cell count was 440/mu L, and the HIV viral load was undetectable in 74%. Of VEGF-A-stained placentas, both decidua and villous endothelium tissue layers were present in 36 (88%). VEGF-A was detected in 31 of 36 (86%) with decidua present, and 39 of 40 (98%) with villous endothelium present. There were no differences in VEGF-A presence in any tissue type by maternal HIV serostatus (P = .28 to >.99). MVM was more common in placentas selected for VEGF-A staining (51 vs 8%; P < .001). Conclusions. VEGF-A immunostaining was highly prevalent, and staining patterns did not differ by maternal HIV serostatus among those with MVM risk factors, indicating that the role of VEGF-A in placental vasculopathy may not differ by maternal HIV serostatus.
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