Further research is needed to elucidate mechanisms for the association of FGS with HIV-1 vulnerability, and these may include schistosome-related impact on mucosal and systemic immunity, including the activation of CD4 trafficking to the genital mucosa (45), or modification in systemic (46) or cervical (20) gene expression, specifically related to the regulation of transcription, the inflammatory response or tissue fibrosis. This evidence concerns the gene CD4 and focal segmental glomerulosclerosis.