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Abstract Our observations in our endemic area showed that not all persons subjected to repeated bilharzial infection and antibilharzial treatment will develop the hepatosplenic syndrome, while others subjected to infection even once and develop hepatosplenic involvement. For this purpose we planned to study the host factors that may lead to immunological and/or genetic susceptibility to develop post schistosomal hepatosplenic syndrome. We investigated the T-cell subsets abnormalities and Hl.A antigen frequencies to single out any difference or association that can indicate different immunologic and/or genetic make up and solve the problem. The study was conducted on two groups of patients: oJ< The first group comprised 15 patients subjected to repeated infection with schistosomiasis mansoni and received antibilharzial therapy but not develop clinically demonstrable hepatosplenic syndrome. oJ< The second group comprised 16 patients who had catched bilharzial infection even once but they develop hepatosplenic involvement. All patients were with no previous or ongoing other disease or drug intake that may alter the immune status. |