Abstract
Innate immunity is one of the main protection mechanisms against viral infections, but how this system works at the maternal-fetal interface, especially during HIV infection, is still poorly known. In this study, we investigated the relationship between pregnancy and innate mechanisms associated with HIV immunity by evaluating the expression of DAMPs, inflammasome components and type I/III IFNs in placenta and serum samples from HIV-infected mothers and exposed newborns. Our results showed that most of these factors, including HMGB1, IL-1, and IFN, were increased in placental villi from HIV-infected mothers. Curiously, however, these factors were simultaneously repressed in serum from HIV-infected mothers and their exposed newborns, suggesting that pregnancy could restrict HIV immune activation systemically but preserve the immune response at the placental level. An effective local antiviral status associated with a suppressed inflammatory environment can balance the maternal immune response, promoting homeostasis for fetal development and protection against HIV infection in neonates.
Highlights
Human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS) are public health problems with high morbidity and mortality rates, with 36.9 million people worldwide estimated to be infected [1]
A residual chronic immune activation persists in HIV-infected patients even when viral replication is efficiently inhibited by antiretroviral therapy (ART) [17]
To assess which scenario would prevail, we evaluated the transcriptional profile of DAMPs S100A8, S100A9, and HMGB1 and their receptors RAGE, TLR4, and TLR9 in HIVinfected placentas (Figure 1)
Summary
Human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS) are public health problems with high morbidity and mortality rates, with 36.9 million people worldwide estimated to be infected [1]. Albeit in maternal HIV infection, infected cells and virions pass through the placenta, either free or associated with neutralizing antibodies, most of HIV-exposed children do not become infected, even without any antiretroviral therapy (ART). These children show a remarkable immune impairment throughout their lives, highlighting the need to better understand the mechanisms involved in HIV infection during pregnancy [2]. The classical innate antiviral system of type I interferons (IFN) is considered a potent inhibitor of HIV infection in CCR5+ CD4+ T cells and macrophages [3]. We still lack a deep in situ understanding of the IFN response in the placental niche during HIV infection
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