These authors contributed equally to the manuscript.
Genetic variation in the interleukin-28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection†
Article first published online: 19 AUG 2011
Copyright © 2011 American Association for the Study of Liver Diseases
Volume 54, Issue 4, pages 1127–1134, October 2011
How to Cite
Marabita, F., Aghemo, A., De Nicola, S., Rumi, M. G., Cheroni, C., Scavelli, R., Crimi, M., Soffredini, R., Abrignani, S., De Francesco, R. and Colombo, M. (2011), Genetic variation in the interleukin-28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection. Hepatology, 54: 1127–1134. doi: 10.1002/hep.24503
Potential conflict of interest : Dr. Rumi received grants from Roche, Janssen, and Gilead. Dr. Colombo advises and received grants from Roche, Merck, Gilead, Bayers, and Bristol-Myers Squibb. He also advises Tibotec.
- Issue published online: 27 SEP 2011
- Article first published online: 19 AUG 2011
- Accepted manuscript online: 30 JUN 2011 07:11PM EST
- Manuscript Accepted: 7 JUN 2011
- Manuscript Received: 18 FEB 2011
Polymorphisms in the interleukin-28B (IL28B) region are associated with spontaneous and treatment-induced viral clearance in hepatitis C virus (HCV) infection. Nevertheless, it is unknown whether genetic variation at the IL28B locus influences the natural history of chronic HCV infection. Thus, we asked whether an association between IL28B polymorphisms and liver fibrosis progression existed. We studied 247 consecutive patients with chronic HCV, an accurate estimate of the date of infection, and a liver biopsy performed before any treatment. No patient had a history of alcohol abuse or coinfection with other viruses. We assessed the role of rs8099917 and rs12979860 polymorphisms and the effect of host and environmental factors on fibrosis progression. Blood transfusion (75%) was the main modality of infection. Median age at infection was 21 years, and median interval between infection and liver biopsy was 25 years. One hundred twenty-nine patients (52%) were infected by HCV-1, 74 (30%) by HCV-2, 34 (14%) by HCV-3, and 10 (4%) by HCV-4. Bridging fibrosis/cirrhosis (Ishak ≥4) was detected in 24% of patients. Age at infection had a marked effect on fibrosis progression by both a linear model and Cox proportional-hazard regression (P < 2E-16). A 12.1% increase in the hazard of advanced fibrosis was estimated for each additional year at infection, suggesting that this was the major explanatory variable in this cohort. Male gender (P < 0.05), HCV genotype 3 (P < 0.001) and steatosis (P < 0.05) were also associated with faster fibrosis progression. Conversely, the two IL28B polymorphisms had no impact on fibrosis progression. Conclusion: In HCV patients with a known date of infection, IL28B genotype was not associated with fibrosis progression rate or with the risk of developing advanced liver fibrosis. (HEPATOLOGY 2011;)