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CD24 polymorphisms affect risk and progression of chronic hepatitis B virus infection
Author(s) -
Li Dongling,
Zheng Linghua,
Jin Lei,
Zhou Yuesu,
Li Haiying,
Fu Junliang,
Shi Ming,
Du Peishuang,
Wang Lizhong,
Wu Hao,
Chen GuoYun,
Zheng Pan,
Liu Yang,
Wang FuSheng,
Wang Shengdian
Publication year - 2009
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.23047
Subject(s) - hepatocellular carcinoma , hepatitis b virus , cirrhosis , cd24 , immunology , allele , medicine , carcinogenesis , hepatitis b , liver cancer , hepatitis c virus , virus , virology , cancer research , biology , cancer , gene , breast cancer , genetics
T‐cell immunity to hepatitis B virus (HBV) is involved in both viral clearance and the pathogenesis of cirrhosis and hepatocellular carcinoma following chronic HBV infection. It is therefore of great interest to analyze whether genetic polymorphism of genes involved in the immune response may determine the outcomes of chronic HBV infection. Here we report that CD24 polymorphisms affect the risk and progression of chronic HBV infection. Thus the CD24 P170 T allele, which is expressed at a higher level, is associated with an increased risk of chronic HBV infection. Among the chronic HBV patients this allele shows recessive association with more rapid progression to liver cirrhosis and hepatocellular carcinoma in comparison to the P170 C allele. In contrast, a dinucleotide deletion at position 1527–1528 (P1527 del ), which reduces CD24 expression, is associated with a significantly reduced risk of chronic HBV infection. To confirm the role for CD24 in liver carcinogenesis, we compared the size of liver tumor developed in CD24 −/− and CD24 +/− HBV transgenic mice. Our data demonstrate that targeted mutation of CD24 drastically reduced the sizes of spontaneous liver cancer in the HBV transgenic mice. Conclusion: These data demonstrate that genetic variation of CD24 may be an important determinant for the outcome of chronic HBV infection. (H EPATOLOGY 2009.)