Table 2.

Antiretroviral Therapy and HIV associated PE.

Antiretroviral Type	Main Findings	References
Nucleoside/nucleotide reverse transcriptase inhibitors	Immune reconstitution Decreased endothelial cell proliferation, migration Elevated mitochondrial oxidative stress Defective tyrosine kinase receptor and VEGFR-2 signalling Increased reactive oxygen species (ROS) generation in trophoblast apoptosis predisposing PE and/or IUGR	[121,122]
Protease inhibitors	Immune reconstitution preluding PE development Decreased progesterone in trophoblast cells impede invasion Dysregulated uterine decidualization and spiral artery remodelling Decreased VEGF, placental growth factor (PlGF), angiopoietin-2, interferon-gamma and matrix metalloproteinase 9 (MMP-9) in decidual cell Uterine natural killer (uNK) cell depletion Incomplete trophoblast cell invasion following decreased expression of the transcription factor STAT3	[123,124,125]
HAART	Immune reconstitution Dysregulated nuclear factor kappa B (NF-κB) transcription factors and, hence, decreased MMP and VEGF expression Increased sFlt-1 and sEng Decreased PlGF and VCAM-1	[83,88,126,127,128,129,130]