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This work was supported by the ��Association Fran?aise contre les Myopathies��, the ��r��gion Pays-de-la-Loire�� (Emergence collective 2012, AGTI-1), and the ��Commissariat g��n��ral �� l'investissement�� (ANR-PGT Investissements d'avenir). Supplementary Material Supplementary Figures and Tables Click here for additional data file.(980K, pdf) Supplementary Table S9 Click here for additional data file.(40K, xls)""HIV-1 transmission via genital mucosal surfaces is an inefficient process with an estimated risk of 3�C50 events per 10,000 sexual exposures or LDK378 and determination of the critical events for successful HIV-1 transmission may help develop better prevention measures. However, examining the early events of successful, natural HIV infection in human subjects is technically challenging. Fortunately, not see more everyone exposed to HIV-1 become infected. In all investigated HIV-exposed cohorts, there are ~10�C15% of these HIV-exposed individuals who remain seronegative (HIV-exposed seronegative (HESN)).4 Studies of molecular events that may be involved in hindering the establishment of HIV infection can be performed in HESN,5,6,7 and the findings will help identifying genetic and immune correlates of protection.8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25 Our earlier work identified interferon (IFN) regulatory factor-1 (IRF-1) to be a genetic and functional correlate of protection against HIV-1 acquisition in a highly HIV-exposed commercial sex worker cohort Quetiapine in Nairobi, Kenya26,27,28; these HESN women can be defined as epidemiologically ��resistant�� to HIV infection.29,30 IRFs are a family of transcriptional regulators found in all principle metazoan groups including simple organisms such as sea sponges.31 IRF genes are thought to have coevolved with Rel/NF-��B genes, which together play important roles in regulating host immunity.32 IRF-1, the first IRF identified, functions as a transcription regulator33 by binding to an IFN-stimulated response element (ISRE), found in numerous genes controlling immune responses and cellular apoptosis.2,31,34 IRF-1 expression is expressed at low basal level in most cell types and can be induced by specific cytokine/chemokines and by viral infection. It was recently shown to be upregulated in CD4+ T cells,35,36 monocyte-derived dendritic cells, and monocyte-derived macrophages37,38 by in vitro HIV infection. In addition to the antiviral role, IRF-1/NF-��B are essential facilitators of the early transactivation of HIV-1 genome.