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Influence of interleukin 12B (IL12B) polymorphisms on spontaneous and treatment-induced recovery from hepatitis C virus infection

Authors :
Mueller, Tobias
Mas-Marques, Andreas
Sarrazin, Christoph
Wiese, Manfred
Halangk, Juliane
Witt, Heiko
Ahlenstiel, Golo
Spengler, Ulrich
Goebel, Uwe
Wiedenmann, Bertram
Schreier, Eckart
Berg, Thomas
Source :
Journal of Hepatology. Oct2004, Vol. 41 Issue 4, p652-658. 7p.
Publication Year :
2004

Abstract

Interleukin-12 (IL-12) governs the Th1-type immune response, affecting the spontaneous and treatment-induced recovery from HCV-infection. We investigated whether the IL12B polymorphisms within the promoter region (4bp insertion/deletion) and the 3′-UTR (1188-A/C), which have been reported to influence IL-12 synthesis, are associated with the outcome of HCV infection.We analyzed 186 individuals with spontaneous HCV clearance, 501 chronically HCV infected patients, and 217 healthy controls. IL12B 3′-UTR and promoter genotyping was performed by Taqman-based assays with allele-specific oligonucleotide probes and PCR-based allele-specific DNA-amplification, respectively.The proportion of IL12B promoter and 3′-UTR genotypes did not differ significantly between the different cohorts. However, HCV genotype 1-infected patients with high baseline viremia carrying the IL12B 3′-UTR 1188-C-allele showed significantly higher sustained virologic response (SVR) rates (25.3% vs. 46% vs. 54.5% for A/A, A/C and C/C) due to reduced relapse rates (24.2% vs. 12% vs. zero % for A/A, A/C and C/C).IL12B 3′-UTR 1188-C-allele carriers appear to be capable of responding more efficiently to antiviral combination therapy as a consequence of a reduced relapse rate. No association of IL12B polymorphisms and self-limited HCV infection could be demonstrated. [Copyright &y& Elsevier]

Details

Language :
English
ISSN :
01688278
Volume :
41
Issue :
4
Database :
Academic Search Index
Journal :
Journal of Hepatology
Publication Type :
Academic Journal
Accession number :
14579452
Full Text :
https://doi.org/10.1016/j.jhep.2004.06.021