In vitro studies have shown that the interaction between DC-SIGN and HIV-1 can enhance short-term viral transfer to other susceptible cell types such as T lymphocytes [14, 15, 36] . Based on these findings, a Trojan horse model has been proposed whereby was compared in CD163+ and CD1632 subsets from infants bearing or not promoter variants and born from HIV-1-negative mothers (HIV-1 Unexposed; p-336T/p-201C group n = 4; p-336C or p-336C/p-201A group n = 11) or from HIV-1-positive mothers (HIV-1 Exposed; p-336T/p-201C group n = 3; p-336C or p-336C/p-201A group n = 6). Results in C and D are mean 6 S.E.M. values of MFI and difference between subsets or variants was calculated with Student's t test. doi:10.1371/journal.pone.0040706.g002 HIV-1 may subvert DC-SIGN-expressing submucosal dendritic cells to promote dissemination from the periphery to the lymphoid tissues [13] . To date, relatively few studies have assessed the potential impact of DC-SIGN polymorphism in adult HIV-1 infection and the findings have not been consistent. While some [29, 37, 38] have found a significant association, others have not [39] [40] [41] . Little is currently known about the mechanisms underlying HIV-1 passage across the placenta. We and others [16, 33, 34] have shown that DC-SIGN is expressed by placental Hofbauer cells. Moreover, the identification of natural and functional DC-SIGN genetic variants associated with an increased risk of IU HIV-1 infection further support the implication of DC-SIGN in HIV-1 dissemination across the placenta. DC-SIGN polymorphism was not associated with IP and PP HIV-1 infections. However, the relatively small number of subjects analysed in the IP (n = 11) and PP (n = 17) groups may have limited the power of the present study to detect any association and therefore we cannot rule out the possibility that DC-SIGN could also contribute to IP and PP transmission of HIV-1.