Abstract
Maternal HIV infection is associated with an increased risk of preterm birth (PTB). However, the mechanisms underlying this increased risk in women with HIV remain poorly understood. In this regard, it is well-established that labor is an inflammatory process and premature activation of the pro-inflammatory signals (associated with labor) can result in preterm labor which can subsequently lead to PTB. HIV infection is known to cause severe immune dysregulation within its host characterized by altered immune profiles, chronic inflammation and eventually, the progressive failure of the immune system. The human placenta comprises different immune cell subsets, some of which play an important role during pregnancy including participating in the inflammatory processes that accompany labor. It is therefore plausible that HIV/antiretroviral therapy (ART)-associated immune dysregulation within the placental microenvironment may underlie the increased risk of PTB reported in women with HIV. Here, we review evidence from studies that point toward the placental origin of spontaneous PTB and discuss possible ways maternal HIV infection and/or ART could increase this risk. We focus on key cellular players in the maternal decidua including natural killer cells, CD4+ T cells including CD4+ regulatory T cells, CD8+ T cells as well as macrophages.
Highlights
Preterm birth (PTB) is defined by the World Health Organisation (WHO) as delivery before 37 completed weeks of gestation [1]
Decidual Natural killer (NK) cells have been shown to display phenotypic and functional shifts in women who have spontaneous vaginal deliveries and decidual NK (dNK) cells become highly cytotoxic in the presence of a number of pathogens including
Decidual macrophages on the other hand are of interest as they are the main HIV R5-tropic target cells in the decidua, but it remains to be determined how HIV impacts the macrophage polarization and function and how this would impact the risk of preterm birth
Summary
Preterm birth (PTB) is defined by the World Health Organisation (WHO) as delivery before 37 completed weeks of gestation [1]. The highest rates of PTB were in low- and middle-income countries (LMICs) in Asia, and sub-Saharan Africa (SSA) which accounted for 12 million PTBs [2]. PTB is a leading cause of mortality as it accounts for ∼8,500,000 deaths in the neonatal period (first 28 days of life) and an estimated 106,000 deaths in children aged 1–59 months, globally [3]. The rates of morbidity and mortality in preterm neonates increase with the decrease in gestational age [4]. The hardest hit in this regard are LMICs, where births occur in facilities lacking the infrastructural resources and expertise to provide quality obstetric and neonatal care
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