الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Hepatitis C virus (HCV) infection is a global health problem that is sometimes complicated by Schistosoma mansoni (S. mansoni) coinfection. Several reports suggest that S. mansoni increases HCV morbidity and chronicity. However, there are limited data examining the impact of S. mansoni co-infection on the outcome of HCV infection. This study examined the effect of Schistosoma infection on HCV clearance, viral load and HCV-specific immune response in coinfected patients and compared it to that of patients infected with HCV infection alone.
In a cross-sectional survey of 370 healthcare workers (HCW), this study examined HCV-RNA loads, HCV genotype and interferon gamma (IFN-γ) production (by ELISpot assay). The 370 subjects included 68 HCW who are infected with both S. mansoni and HCV, 73 HCV-infected patients and 229 HCW infected with S. mansoni alone. The average (±SEM) HCV-RNA load in co-infected and HCV patients was 1.40±0.27x106 and 1.63±0.25x106 IU/ml, respectively (p=0.252). Only 16 HCW (23.5%) of the co-infected and 24 (32.9%) of the HCV-infected patients spontaneously resolved HCV infection (p=0.297) suggesting no impact of Schistosoma infection on HCV resolution.
HCV genotype 4 prevailed all but one of the infections. In viremic patients, the mean IFN-γ spot forming cells/106 PBMCs (±SEM) among co-infected (n=20) and HCV infected patients (n=14) was 327±105 and 481±138 (p=0.373) while among those without viremia it was 595±229 (n=7) and 232±49 (n=15; p=0.043), respectively. In conclusion, there was no statistical difference in HCV spontaneous resolution or viral load in patients infected with HCV alone or those co-infected with S. mansoni
suggesting that schistosomiasis does not affect the outcome of HCV infection.