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Interleukin-1, interleukin-10 and tumour necrosis factor-alpha gene polymorphisms in hepatitis C virus infection: an investigation of the relationships with spontaneous viral clearance and response to alpha-interferon therapy

Lookup NU author(s): Dr Peter Donaldson

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Abstract

Background/Aims: Though there is a consensus that the HLA DQB1 *0301 allele is important in untreated HCV clearance, this association is not universal and a number of genes outside the major histocompatibility complex may also play a role in host responses to HCV infection. Prime candidates, at present, are the genes encoding pro-inflammatory and immuno-regulatory cytokines. The aim of this study was to investigate the relationship between a number of these candidate genes and both spontaneous and treatment related clearance of hepatitis C virus infection. Methods: Three members of the interleukin-1 gene family: IL-1A , IL-1B and IL-1RN , three polymorphic sites in the interleukin-10 gene promoter (- 1082, - 819, - 592) and two in the tumour necrosis factor-alpha promoter (- 308, - 238) were studied in two independent DNA banks, each with appropriate controls. Standard PCR-based genotyping techniques were used. Results: No significant difference in the distribution of any of the polymorphisms was found in either study set. Conclusions: These findings in two large groups suggest that future investigations should focus on other candidate genes and may support the view that MHC-encoded susceptibility to chronic HCV infection may be determined by MHC class II rather than MHC class III genes.


Publication metadata

Author(s): Constantini PK, Wawrzynowicz-Syczewska M, Clare M, Boron-Kaczmarska A, McFarlane IG, Cramp ME, Donaldson PT

Publication type: Article

Publication status: Published

Journal: Liver

Year: 2002

Volume: 22

Issue: 5

Pages: 404-412

ISSN (print): 1478-3223

ISSN (electronic): 1478-3231

Publisher: Wiley-Blackwell Publishing, Inc.

URL: http://dx.doi.org/10.1034/j.1600-0676.2002.01553.x

DOI: 10.1034/j.1600-0676.2002.01553.x


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