Published in:
01-08-2015 | Original Article—Liver, Pancreas, and Biliary Tract
Association of serum IFN-λ3 with inflammatory and fibrosis markers in patients with chronic hepatitis C virus infection
Published in: Journal of Gastroenterology | Issue 8/2015
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Background
Hepatitis C virus (HCV) is one of the major causes of liver cancer. The single nucleotide polymorphisms within the IFNL3 gene, which encodes interferon (IFN)-λ3, are strongly associated with the response to pegylated IFN-α (PEG-IFN-α) plus ribavirin (RBV) therapy in chronic hepatitis C (C-CH) patients. However, the roles of IFN-λ3 in chronic HCV infection are still elusive. In this study, we aimed to identify clinical and immunological factors influencing IFN-λ3 and evaluated whether serum IFN-λ3 levels are involved or not involved in the response to PEG-IFN-α plus RBV therapy.
Methods
We enrolled 119 C-CH patients with HCV genotype 1 infection who underwent 48 weeks of PEG-IFN-α plus RBV therapy. As controls, 23 healthy subjects and 56 patients with non-HCV viral hepatitis were examined. Serum IFN-λ3 was quantified by chemiluminescence enzyme immunoassay, and 27 cytokines or chemokines were assayed by the multiplexed BioPlex system.
Results
Serum IFN-λ3 levels were higher in C-CH patients or acute hepatitis E patients than in healthy volunteers. Such levels did not differ between the IFNL3 genotypes. In C-CH patients, serum IFN-λ3 was positively correlated with aspartate aminotransferase, alanine aminotransferase, α-fetoprotein, histological activity, fibrosis index, IFN-γ-inducible protein 10, and platelet-derived growth factor. Multivariate analysis showed that IFNL3 single nucleotide polymorphisms, fibrosis score, and macrophage inflammatory protein 1α were involved in the sustained viral clearance in PEG-IFN-α plus RBV therapy; however, serum IFN-λ3 levels were not involved.
Conclusion
Serum IFN-λ3 levels are increased in C-CH patients regardless of the IFNL3 genotype. IFN-λ3 is a biomarker reflecting the activity and fibrosis of liver disease, but is not correlated with the responsiveness to PEG-IFN-α plus RBV therapy.