RESUMO
Patients coinfected with hepatitis C virus [HCV]and schistosomiasis exhibit a unique clinical, virological and histological pattern manifested by viral persistence with high HCV- RNA viral load, higher incidence of cirrhosis, hepatocellular carcinoma, poor response to interferon therapy compared with patients infected with HCV without concomitant schistosomiasis. The aim of the present work was to estimate HCV-RNA viral load, the serum level of interleukin- 10[IL-10] and interferon-gamma [IFN-gamma] in patients with only HCV infection, in patients with only Schistosoma mansoni infestation and in those patients with combined infections and to study any possible correlations. The current study was carried out on [69] of chronic HCV liver disease patients and [18] healthy individuals as a control. Patients were selected from Inpatients and Outpatients of Tropical Medicine and Infectious Diseases Department, Tanta University Hospitals. Patients in this study were subjected to the following: Thorough clinical examination, and lab investigations including; liver function tests, estimation of HCV- RNA viral load by real time PCR and estimation of serum level of IL-10 and IFN-gamma by ELISA. The present study showed that: There was marked and significant increase in the serum level of IL-10 in patients with schistosomiasis and in coinfected patients compared with control group. A significant but mild increase in the serum level of IL-10 was also found in HCV patients compared to control. Regarding IFN-gamma, patients infected with HCV had significant and marked increase in the level of IFN-gamma compared with control and with patients with schistosomiasis and coinfected patients
Conclusions: Schistosoma mansoni infestation seems to induce a Th2-related cytokines with increase in serum levels of IL-10 even in the presence of HCV coinfection. Schistosomiasis may downregulate the stimulatory effect of HCV on Th1 cytokines, leading to inhibition of release of IFN-gamma; and this may lead to the chronicity of HCV infection, hence the poor response to interferon therapy