ABSTRACT
The aim of this study was to investigate the effect of infection with S. mansoni on the balance between Th-1 and Th-2 cytokines in patients with chronic hepatitis C virus [HCV] infection and to show the relations between these two groups of cytokines to the degrees of viral load in these patients. 44 individuals were classified into 4 groups: group I of control subjects [n=10], group II of patients with S. mansoni mono-infection [n=9], group III of patients with chronic HCV mono-infection [n=13] and group IV of patients with both S. mansoni and HCV co-infection [n=12]. For individuals of all studied groups, interferon-gamma and IL-2 [cytokines of Th-1 cells] and IL-4 and IL-10 [cytokines of Th-2 cells] were measured. Viral load was measured for patients of group III [HCV mono-infection] and group IV [co-infected patients]. The results showed that Th-1 cytokines [IFN-gamma and IL-2] were significantly higher in HCV mono-infection patients and significantly lower in patients co-infected with HCV and S. mansoni compared to normal subjects group. In S. mansoni mono-infection group, IFN-gamma was decreased while IL-2 was normal compared to normal control group. Th-2 cytokines [IL-4 and IL-10] were significantly higher in the three patients groups compared to the control group but the degree of increase of IL-4 showed no significant difference between S. mansoni mono-infection patients and HCV mono-infection patients while the degree of increase of IL-10 was higher in S. mansoni mono-infection patients compared to HCV monoinfection patients. The degree of increase of both IL-4 and IL-10 was significantly higher in the coinfection patients compared to the HCV mono-infection patients. Viral load was significantly higher in the co-infected group compared to HCV mono-infection group and in both groups, the viral load was positively correlated with Th-2 cytokines and negatively correlated with Th-1 cytokines [except IL-2 in the group of HCV mono-infection patients]. In conclusion, these results suggest that HCV patients co-infected with S. mansoni suffer from strong activation of Th-2 cells and so increase of Th-2 cytokines that suppress Th-1 cells and related cytokines which is the type of immune response needed in face of HCV. This Th-1/Th-2 imbalance allows more viral replication and higher viral load in these patients compared to HCV patients who are not co-infected with S. mansoni and this may give an explanation to the rapid hepatic deterioration of these co-infected patients