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Schistosome infections are renowned for their ability to induce regulatory networks such as regulatory T cells (Treg) that control immune responses against homologous and heterologous antigens such as allergies. However, in the case of co-infections with hepatitis C virus ( HCV), schistosomes accentuate disease progression and we hypothesized that expanding schistosome-induced Treg populations change their phenotype and could thereby suppress beneficial anti- HCV responses. We therefore analysed effector T cells and n/ iTreg subsets applying the markers Granzyme B (GrzB) and Helios in Egyptian cohorts of HCV mono-infected ( HCV), schistosome-co-infected ( Sm/ HCV) and infection-free individuals. Interestingly, viral load and liver transaminases were significantly elevated in Sm/ HCV individuals when compared to HCV patients. Moreover, overall Treg frequencies and HeliosposTreg were not elevated in Sm/ HCV individuals, but frequencies of GrzB+Treg were significantly increased. Simultaneously, GrzB+ CD8+ T cells were not suppressed in co-infected individuals. This study demonstrates that in Sm/ HCV co-infected cohorts, liver disease is aggravated with enhanced virus replication and Treg do not expand but rather change their phenotype with GrzB possibly being a more reliable marker than Helios for iTreg. Therefore, curing concurrent schistosome disease could be an important prerequisite for successful HCV treatment as co-infected individuals respond poorly to interferon therapy. [ABSTRACT FROM AUTHOR]