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Tumor necrosis factor alpha promoter polymorphism at position ‐238 is associated with chronic active hepatitis C infection
Author(s) -
Höhler Thomas,
Kruger Anke,
Gerken Guido,
Schneider Peter M.,
zum Büschenfelde KarlH. Meyer,
Rittner Christian
Publication year - 1998
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/(sici)1096-9071(199803)54:3<173::aid-jmv5>3.0.co;2-2
Subject(s) - biology , linkage disequilibrium , allele , haplotype , locus (genetics) , major histocompatibility complex , human leukocyte antigen , promoter , gene , allele frequency , virology , immunology , microbiology and biotechnology , genetics , gene expression , antigen
Tumor necrosis factor α (TNF‐α) is involved in the pathogenesis of chronic hepatitis C virus infection. The gene for TNF‐α is encoded in the major histocompatibility locus (MHC). Two polymorphisms at positions ‐308 and ‐238 in the TNF‐α promoter region might influence TNF‐α expression. These promoter polymorphisms have been linked previously to a number of infectious diseases. TNF‐α promoter polymorphisms at positions ‐238 and ‐308 were studied by DNA sequencing and sequence‐specific oligonucleotide hybridization in 82 individuals with chronic hepatitis C and 99 control subjects. Subjects had been HLA class I and class II typed in a previous study. The frequency of the TNF238.2 promoter allele was significantly higher in the hepatitis C group (18.7%) compared to the controls (3.5%; P < 0.0001; pcorr < 0.009). No significant differences in the frequency of the TNF308.2 allele were observed between patients and controls. The increased frequency of the TNF238.2 allele could not be explained by linkage disequilibrium to HLA‐B or ‐DR genes. These findings show an association between the TNF238.2 promoter variant and chronic active hepatitis C. They suggest that this polymorphism or a linked gene may be a host factor contributing to the development of chronic active hepatitis C. J. Med. Virol. 54:173–177, 1998. © 1998 Wiley‐Liss, Inc.