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|Title:||Immunodeficiency to hepatitis B virus infection and genetic susceptibility to development of hepatocellular carcinoma||Authors:||Simons, M.J.
|Issue Date:||1975||Citation:||Simons, M.J., Yu, M., Shanmugaratnam, K. (1975). Immunodeficiency to hepatitis B virus infection and genetic susceptibility to development of hepatocellular carcinoma. Annals of the New York Academy of Sciences Vol. 259 : 181-195. ScholarBank@NUS Repository.||Abstract:||The high frequency of hepatitis B antigen (HB(s)Ag) in hepatocellular carcinoma (HCC) patients has led to the hypothesis that immunoresponsiveness to hepatitis B virus (HBV) may be deficient in some patients, and that the immune response deficiency may have a genetic basis. Radioelectrocomplexing (REC), a radioimmunoassay in gel based on the principle of counterimmunoelectrophoresis (CIE), has been used to identify four HBV immune status subgroups: 1) HB(s)Ag+ve/HB(s)Ab+ve; 2) HB(s)Ag+ve/HB(s)Ab-ve; 3) HB(s)Ag-ve/HB(s)Ab+ve; 4) HB(s)Ag-ve/HB(s)Ab-ve/HB(s)Ab -ve. These subgroups comprise 2, 6, 70, and 22%, respectively, among blood donors, and 32, 19, 23, and 26%, respectively, among HCC patients. Although the HBV exposure rates in the two groups were similar, the immune complexemic rates and HB(s) antigenemic rates were significantly higher in HCC patients than in the blood donors. It is proposed that the failure of termination of HBV infection revealed by these high rates reflects an immunodeficiency state characterized by an inability to produce high avidity HB(s)Ab. The immunodeficiency might have a primary genetic basis, or it might be secondary to the immunodepressive effects of concurrent viral or parasitic infections.||Source Title:||Annals of the New York Academy of Sciences||URI:||http://scholarbank.nus.edu.sg/handle/10635/133413||ISSN:||00778923|
|Appears in Collections:||Staff Publications|
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