6533b822fe1ef96bd127cdfe
RESEARCH PRODUCT
A tumor necrosis factor-alpha (TNF-alpha) promoter polymorphism is associated with chronic hepatitis B infection.
SchneiderMeyer Zum BüschenfeldeHöhlerKrugerGerkenRittnersubject
Linkage disequilibriumHepatitis B virusGenotypemedicine.medical_treatmentImmunologyBiologymedicine.disease_causeVirusLinkage DisequilibriumHepatitis B ChronicmedicineImmunology and AllergyHumansInterferon gammaProspective StudiesPromoter Regions GeneticAllelesHepatitis B virusPolymorphism GeneticTumor Necrosis Factor-alphaPromoterVirologyChronic infectionCytokineImmunologyOriginal ArticleViral diseasemedicine.drugdescription
SUMMARY Cytokines such as TNF-α and interferon gamma (IFN-γ) are important for the elimination of infected hepatocytes during acute hepatitis B virus (HBV) infection. Two G versus A transitions in the TNF-α promoter region at positions −308 and −238 possibly influence TNF-α expression. We investigated these TNF-α polymorphisms in 71 patients with chronic HBV infection, in 32 subjects that had spontaneously recovered from acute HBV infection, and in 99 healthy controls. The −238 A promoter variant was present in 18 (25%) of 71 patients with chronic HBV infection compared with two (6%) of 32 subjects with acute infection (P < 0.04), and seven (7%) of 99 controls (P < 0.003). By contrast, the prevalence of the variant at position −308 was similar in all investigated groups. The observed differences could not be explained by linkage disequilibrium to HLA-B or -DRB1* alleles. These findings suggest an association between the TNF-α promoter polymorphism at position −238 and the development of chronic HBV infection. This promoter variant appears to be linked to defective viral clearance.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1998-03-01 | Clinical and experimental immunology |