Lethal disease in Schistosoma mansoni infections is mostly due to portal hypertension caused by hepatic periportal fibrosis. To evaluate the factors that may determine severe disease, livers and spleens were examined by ultrasound in a Sudanese population living in a village where S. mansoni is endemic. Early (FI), moderate (FII), or advanced (FIII) fibrosis was observed in 58%, 9%, and 3% of the population, respectively. Although FI affected 50%-70% of the children and adolescents, FII prevalence was low in subjects

Schistosome infection is a major public health concern affecting millions of people living in tropical regions of Africa, Asia, and South America. Schistosomes cause mild clinical symptoms in most subjects, whereas a small proportion of individuals presents severe clinical disease (as periportal fibrosis (PPF)) that may lead to death. Severe PPF results from an abnormal deposition of extracellular matrix proteins in the periportal spaces due to a chronic inflammation triggered by eggs and schistosome Ags. Extracellular matrix protein production is regulated by a number of cytokines, including IFN-γ. We have now screened putative polymorphic sites within this gene in a population living in an endemic area for Schistosoma mansoni. Two polymorphisms located in the third intron of the IFN-γ gene are associated with PPF. The IFN-γ +2109 A/G polymorphism is associated with a higher risk for developing PPF, whereas the IFN-γ +3810 G/A polymorphism is associated with less PPF. The polymorphisms result in changes in nuclear protein interactions with the intronic regions of the gene, suggesting that they may modify IFN-γ mRNA expression. These results are consistent with the results of previous studies. Indeed, PPF is controlled by a major locus located on chromosome 6q22-q23, closely linked to the gene encoding the α-chain of the IFN-γ receptor, and low IFN-γ producers have been shown to have an increased risk of severe PPF. Together, these observations support the view that IFN-γ expression and subsequent signal transduction play a critical role in the control of PPF in human hepatic schistosome infection (S. mansoni).

This study shows that prevalence of HBV infection is high in the studied population and it is hoped that introduction of blood screening and vaccination against HBV would decrease the carrier pool in the next few years.

This is a cross sectional study carried out in Gezira state of central Sudan, an area with a high prevalence of Schistosoma mansoni infection, to determine the prevalence of hepatitis C virus (HCV) antibodies and risks factors for HCV infection. A total of 410 subjects in Um Zukra village were tested for HCV antibodies, 2.2% were reactive. The prevalence was highest in those between 11 and 20 years old with equal prevalence among males and females. No correlation was found between HCV infection and S. mansoni infection or parenteral antischistosomal therapy. It was concluded that HCV infection is of low seroprevalence and that schistosomiasis and parenteral antischistosomal therapy are not major risk factors for infection in the population studied.

An association study of a cohort of 177 Sudanese patients infected with Schistosoma mansoni [82 (46%) males and 95 (54%) females] was conducted to evaluate the factors controlling the regression of liver fibrosis 39 months after treatment with praziquantel using ultrasound evaluation. Periportal fibrosis (PPF) was regressed in 63 (35.6%) patients, while the disease progressed to higher grades in 24 (13.6%) patients. The grade of PPF did not change in 90 (50.8%) patients. The mean values of portal vein diameter, splenic vein diameter and index liver size in subjects in whom PPF regressed after treatment were significantly lower than in subjects in whom the disease was progressed (P<0.0001, P=0.031 and P=0.003, respectively). The progression of hepatic fibrosis in males (15, 8.5%) was greater than that in females (9, 5.1%). Patients with regression or progression phenotypes tend to cluster in certain families. Our study indicated that regression, progression and stabilization of PPF after praziquantel therapy is controlled by gender, age, grade of fibrosis and possibly inherited factors.