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Association of genetic variations in CCR5 and its ligand, RANTES with clearance of hepatitis B virus in Korea
Author(s) -
Ahn Sang Hoon,
Kim Do Young,
Chang Hye Young,
Hong Sun Pyo,
Shin JeonSoo,
Kim Yu Seun,
Kim Hyejin,
Kim Ja Kyung,
Paik Yong Han,
Lee Kwan Sik,
Chon Chae Yoon,
Moon Young Myoung,
Han KwangHyub
Publication year - 2006
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20739
Subject(s) - chemokine receptor ccr5 , hepatitis b virus , virology , biology , virus , chemokine , cc chemokine receptors , immunology , genotype , promoter , chemokine receptor , gene , inflammation , genetics , gene expression
Immunogenetic factors may play a role in determining the susceptibility of an individual to viral infection. The aim of current study was to investigate the association of clearance of hepatitis B virus (HBV) with promoter polymorphisms within the CC chemokine receptor 5 (CCR5) and its major ligand, regulated upon activation, normal T cells expressed and secreted (RANTES) genes. Five chemokine system polymorphisms (CCR5 Δ32, CCR5 promoter 59029G/A, 59353C/T, RANTES −403G/A, and −28C/G) were studied in a total of 698 subjects. The carriage of each genetic variant was compared among “spontaneously recovered” group (n = 243), “chronic carrier” group (n = 349), and “unexposed” group (n = 106). CCR5 59029G promoter variant was associated with clearance of HBV infection in an acute phase (OR = 1.71, P = 0.006, dominant model; OR = 2.17, P < 0.001, recessive model) and amelioration of hepatic inflammation ( P = 0.003) with the control of HBV replication ( P = 0.04) in chronic carriers. Interestingly, CCR5 59029 was linked completely to CCR5 59353, and CCR5 Δ32 homozygosity or heterozygosity was not found in any Korean patient. No association was seen with RANTES polymorphisms at position −403 and −28. The CCR5 59029G/CCR5 59353T polymorphism may play a role in the clearance of HBV infection. J. Med. Virol. 78:1564–1571, 2006. © 2006 Wiley‐Liss, Inc.