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Hepat Mon. 2014 Oct 1;14(10):e22649. doi: 10.5812/hepatmon.22649. eCollection 2014 Oct.

The Impact of IFNL4 rs12979860 Polymorphism on Spontaneous Clearance of Hepatitis C; A Case-Control Study.

Author information

1
Iran Hepatitis Network, Tehran, IR Iran ; Middle East Liver Disease (MELD) Center, Tehran, IR Iran ; Armin Pathobiology Laboratory, Tehran, IR Iran.
2
Iran Hepatitis Network, Tehran, IR Iran ; Middle East Liver Disease (MELD) Center, Tehran, IR Iran.
3
Iran Hepatitis Network, Tehran, IR Iran ; Armin Pathobiology Laboratory, Tehran, IR Iran ; Department of Genetics, Islamic Azad University-Arsanjan Branch, Arsanjan, IR Iran.
4
Iran Hepatitis Network, Tehran, IR Iran ; Middle East Liver Disease (MELD) Center, Tehran, IR Iran ; Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, IR Iran.

Abstract

BACKGROUND:

About 30% of individuals with hepatitis C virus (HCV) infection are able to clear HCV spontaneously. Differences in host genetics affect the outcome of HCV infection. Single nucleotide polymorphisms (SNPs) of the Interferon lambda (IFNL) genes were associated with spontaneous and treatment-induced clearance of HCV infection.

OBJECTIVES:

The aim of this study was to evaluate the association between the IFNL4 rs12979860 SNP and spontaneous clearance of HCV infection in Iranian population.

MATERIALS AND METHODS:

A case-control study was designed on 91 cases with spontaneous HCV infection clearance and 259 patients with persistent HCV infection as the control group. The rs12979860 SNP was assessed as the most common IFNL polymorphism by PCR-RFLP method.

RESULTS:

Distribution of rs12979860 CC genotype in the spontaneous clearance group was around two folds of its distribution in chronic hepatitis C group (P < 0.001, OR = 4.09, 95% CI = 2.44-6.86).

CONCLUSIONS:

The rs12979860 SNP was observed as a strong host genetic factor associated with spontaneous clearance of hepatitis C infection.

KEYWORDS:

Genetic polymorphism; Hepatitis C; Human IFNL4 Protein

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