01623nas a2200229 4500000000100000008004100001260001200042653002800054653003500082653006900117653004300186100001200229700001100241700001400252700001200266700001600278245010500294856016700399300001100566520080200577022001401379 2020 d c05/202010aSchistosoma haematobium10aSexually transmitted infection10aUrogenital schistosomiasis, Vaginal or cervicovaginal microbiota10aVaginal or cervicovaginal inflammation1 aSturt A1 aWebb E1 aFrancis S1 aHayes R1 aBustinduy A00aBeyond the barrier: Female Genital Schistosomiasis as a potential risk factor for HIV-1 acquisition. uhttps://reader.elsevier.com/reader/sd/pii/S0001706X19314391?token=725AE7FAB47B059FDAE841D5877717B45CB40DC28BB0259F9A85652321A5CFAB65733191CA5461F885B08FD873281C9D a1055243 a

Female genital schistosomiasis (FGS) results from egg-deposition in the female reproductive tract primarily by the waterborne parasite Schistosoma (S.) haematobium, and less commonly by Schistosoma (S.) mansoni. FGS affects an estimated 20-56 million women worldwide, mostly in sub-Saharan Africa. There is cross-sectional evidence of increased HIV-1 prevalence in schistosomiasis-infected women, but a causal relationship between FGS and either HIV-1 acquisition or transmission has not been fully established. Beyond the pathognomonic breach in the cervicovaginal barrier caused by FGS, this narrative review explores potential mechanisms for a synergistic relationship between S. haematobium infection, FGS, and HIV-1 acquisition through vaginal inflammation and target cell recruitment.

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