Background: Few studies focused on the study of blood groups in Gabon. This study aimed to determine the phenotypic frequency of ABO and Rhesus antigens in blood donors of Libreville and to assess the association between ABO blood groups and transfusion-transmitted infections.Materials and Methods: The study of ABO and Rhesus blood groups concerned 4,744 blood donors. ABO and Rhesus phenotyping were obtained using monoclonal monospecific antisera: anti-A, anti-B, anti-AB, anti-D, anti-E, anti-C, anti-c, and anti-e with an automate (QWALYS® 3, DIAGAST, France) or a card gel (ID Card, BIO-RAD) according to manufacturer’s instructions.Results: The phenotypic frequency of blood group antigens A, B, AB and O were respectively 21.0%; 17.6%; 2.6% and 58.9%. Those of rhesus antigens D, d, C, c, E and e were 97.7%; 2.3%; 15.9%; 99.9%; 17.6%; 99.3%, respectively. The prevalence of ABO and Rh antigens in Gabonese donors reported here are significantly different from those of neighboring countries. No association was found between the prevalence of HIV, HCV and syphilis and ABO blood groups. Instead, HBV seroprevalence was twice as high among non-O blood groups donors compared with blood group O donors [OR = 2 (CI 1.26 to 3.2), p = 0.003].Conclusions: This study provides new data on phenotypic frequency of ABO and Rh blood groups in a representative sample of the Gabonese blood donor population. It suggests a significant association between ABO blood group and HBV infection.

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The Aryl hydrocarbon receptor (AhR) identifies “non-pathogenic” Th17-polarized CD4+T-cells in autoimmune models. Thus, we explored whether AhR restricts HIV-1 in Th17-cells, consistent with its antiviral role in macrophages. AhR-specific CRISPR/Cas9-mediated knockout and pharmacological blockade decreased AhR target gene expression (CYP1A1/IL-22/IL-17A/IL-10/ ITGB7), while increasing HIV-1 replication in CD4+T-cells. Pharmacological AhR activation caused opposite effects. AhR agonism/antagonism modulated HIV-1 replication mainly in Th17/Th22-polarized CCR6+CD4+T-cells. Single-round VSV-G-pseudotyped HIV-1 infection demonstrated that AhR acts at post-entry levels, with AhR blockade increasing the efficacy of early/late reverse transcription steps and subsequently integration/translation. In viral outgrowth assay, the AhR blockade boosted the detection of replication-competent viral reservoirs in CD4+T-cells of people living with HIV-1 (PLWH) receiving antiretroviral therapy (ART). Finally, RNA-Sequencing revealed genes/pathways modulated by AhR blockade in CD4+T-cells of ART-treated PLWH, with known HIV-1 interactor activities (NCBI HIV Interactor Database) and AhR responsive elements in their promoters (ENCODE). Among them, HIC1, a repressor of Tat-mediated HIV-1 transcription and a tissue-residency inducer, represents a putative AhR mechanism of action. These results demonstrate that AhR governs an antiviral transcriptional program in CD4+T-cells and point to the use of AhR inhibitors to boost viral outgrowth in “shock and kill” HIV-1 remission/cure strategies.BRIEF SUMMARYWe identified the aryl hydrocarbon receptor as a barrier to HIV-1 infection/outgrowth in Th17-polarized CD4+T-cells and a novel therapeutic target in HIV-1 cure/remission interventions.