The frequency of early in utero mother-to-child transmission (MTCT) is low even in the absence of antiretroviral therapy. One route of HIV-1 in utero transmission is the infection of cells at the materno-fetal interface. In fact the decidua is susceptible to HIV-1 infection. At the materno-fetal interface, decidual cells are in contact with the placenta, which can be infected in vitro by cellular contact with infected cells. Thereby, infected decidual cells or maternal blood cells could infect the placenta in vivo. However, several mechanisms involved in the control of HIV-1 infection have been described in the placenta and in the decidua. Notably, the balance of cytokine and chemokine expression profile influences HIV-1 infection. Other soluble factors, like hormones and antibodies, are involved in the control of the placenta infection. Finally, decidual immune cells, such as NK cells or T cells subsets, could also be involved in the control of HIV-1 MTCT. However their role in this context has not been studied yet. The understanding of these mechanisms of control is important for the development of new prevention strategies against HIV-1 transmission.
Keywords: HIV-1, transmission, mother-to-child transmission, in utero transmission, mucosa, placenta, decidua, trophoblast cells, Hofbauer cells, choriocarcinoma, Natural killer, Antigen presenting cells, mucosal immunity, control, crosstalk, soluble factors, cytokines, co-infection, materno-fetal interface, pregnancy.