Beyond the barrier: Female Genital Schistosomiasis as a potential risk factor for HIV-1 acquisition

Highlights

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  FGS is associated with prevalent HIV-1 infection.

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  Characteristic FGS lesions may allow HIV-1 access to sub-epithelial target cells

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  Cervical egg granulomas bring together the target cells needed for HIV-1 infection

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  S. haematobium has been associated with altered systemic/genital cytokine levels

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  HIV-1 RNA concentrations may be altered in HIV-1 and schistosomiasis coinfection

Abstract

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.

Graphical abstract

Female Genital Schistosomiasis and HIV-1 acquisition may be associated through vaginal inflammation, barrier dysfunction, and target cell recruitment.