HIV-1 at the placenta: immune correlates of protection and infection

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Purpose of review

Mother-to-child transmission (MTCT) of HIV-1 remains a significant global health concern despite implementation of maternal combination antiretroviral therapy for treatment as prevention to offset transmission. The risk of in-utero HIV-1 transmission in the absence of interventions is ∼7%. This low rate of transmission points to innate and adaptive mechanisms to restrict lentiviral infection within the placenta.

Recent findings

Placental macrophages (Hofbauer cells) are key mediators in in-utero transmission of HIV-1. Hofbauer cells constitutively express elevated concentrations of regulatory cytokines, which inhibit HIV-1 replication in vitro, and possess intrinsic antiviral properties. Hofbauer cells sequester HIV-1 in intracellular compartments that can be accessed by HIV-1-specific antibodies and may occur in vivo to offset MTCT. Intriguingly, studies have reported strong associations between maternal human cytomegalovirus (HCMV) viremia and MTCT of HIV-1. HCMV infection at the placenta promotes inflammation, chronic villitis, and trophoblast damage, providing potential HIV-1 access into CD4+CCR5+ target cells. The placenta exhibits a variety of mechanisms to limit HIV-1 replication, yet viral-induced activation with maternal HCMV may override this protection to facilitate in-utero transmission of HIV-1.


Understanding immune correlates of protection or transmission at the placenta during on-going HIV-1 exposure may contribute to understanding HIV pathogenesis and the development of effective immunotherapies.

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