Antigen-Presenting Cells Represent Targets for R5 HIV-1 Infection in the First Trimester Pregnancy Uterine Mucosa |
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Authors: | Romain Marlin Marie-Thérèse Nugeyre Claire de Truchis Nadia Berkane Amélie Gervaise Fran?oise Barré-Sinoussi Elisabeth Menu |
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Affiliation: | 1. Institut Pasteur, Regulation of Retroviral Infection Unit, Department of Virology, Paris, France.; 2. Gynecology-Obstetrics Service, A. Béclère Hospital, AP-HP, Clamart, France.; 3. Department of Gynecology Obstetrics and Reproductive Medecine, Tenon Hospital, AP-HP, UMPC, Paris, France.;Comprehensive AIDS Reseach Center, China |
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Abstract: |
BackgroundDuring the first trimester of pregnancy, HIV-1 mother-to-child transmission is relatively rare despite the permissivity of placental cells to cell-to-cell HIV-1 infection. The placenta interacts directly with maternal uterine cells (decidual cells) but the physiological role of the decidua in the control of HIV-1 transmission and whether decidua could be a source of infected cells is unknown.Methodology/Principal FindingsTo answer to this question, decidual mononuclear cells were exposed to HIV-1 in vitro. Decidual cells were shown to be more susceptible to infection by an R5 HIV-1, as compared to an X4 HIV-1. Infected cells were identified by flow cytometry analysis. The results showed that CD14+ cells were the main targets of HIV-1 infection in the decidua. These infected CD14+ cells expressed DC-SIGN, CD11b, CD11c, the Fc gamma receptor CD16, CD32 and CD64, classical MHC class-I and class-II and maturation and activation molecules CD83, CD80 and CD86. The permissivity of decidual tissue was also evaluated by histoculture. Decidual tissue was not infected by X4 HIV-1 but was permissive to R5 HIV-1. Different profiles of infection were observed depending on tissue localization.Conclusions/SignificanceThe presence of HIV-1 target cells in the decidua in vitro and the low rate of in utero mother-to-child transmission during the first trimester of pregnancy suggest that a natural control occurs in vivo limiting cell-to-cell infection of the placenta and consequently infection of the fetus. |
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