Interferon (IFN)-γ-inducible protein-10: Association with histological results, viral kinetics, and outcome during treatment with pegylated IFN-α2a and ribavirin for chronic hepatitis C virus infection

Ana I. Romero, Martin Lagging, Johan Westin, Amar P. Dhillon, Lynn B. Dustin, Jean Michel Pawlotsky, Avidan U. Neumann, Carlo Ferrari, Gabriele Missale, Bart L. Haagmans, Solko W. Schalm, Stefan Zeuzem, Francesco Negro, Elke Verheij-Hart, Kristoffer Hellstrand

Research output: Contribution to journalArticlepeer-review

202 Scopus citations

Abstract

Background. We investigated associations between interferon (IFN)-γ-inducible protein (IP)-10 and liver histological results, viral kinetic response, and treatment outcome in patients infected with hepatitis C virus (HCV) genotypes 1-4. Methods. Plasma IP-10 was monitored before, during, and after treatment with pegylated IFN-α2a and ribavirin in 265 HCV-infected patients. Results. In univariate analyses, a low baseline IP-10 level was significantly associated with low baseline viral load, rapid viral response (RVR), a sustained viral response (SVR), body mass index <25 kg/m2, and less-pronounced fibrosis, inflammation, and steatosis (for HCV genotypes other than 3). When the results of the univariate analyses were included in multivariate analyses, a low plasma IP-10 level, low baseline viral load, and genotype 2 or 3 infection were independent predictors of an RVR and SVR. IP-10 levels decreased 6 weeks into treatment and remained low in patients with an SVR. By contrast, plasma levels of IP-10 rebounded in patients who had detectable HCV RNA after the completion of treatment. Using cutoff IP-10 levels of 150 and 600 pg/mL for predicting an SVR in patients infected with HCV genotype 1 yielded a specificity and sensitivity of 81% and 95%, respectively. Conclusion. Baseline IP-10 levels are predictive of the response to HCV treatment.

Original languageEnglish
Pages (from-to)895-903
Number of pages9
JournalJournal of Infectious Diseases
Volume194
Issue number7
DOIs
StatePublished - 1 Oct 2006

Bibliographical note

Funding Information:
Received 3 February 2006; accepted 19 May 2006; electronically published 29 August 2006. Presented in part: 12th International Symposium on Hepatitis C Virus and Related Viruses, Montreal, Canada, 2–6 October 2005 (abstract O-07). Potential conflicts of interest: none reported. Financial support: European Community (grant QLK2-2000-00836); Swedish Society against Cancer; Hoffmann–La Roche; Maxim Pharmaceuticals. Reprints or correspondence: Dr. Martin Lagging, Depts. of Virology and Infectious Diseases, Guldhedsgatan 10B, SE-413 46 Göteborg, Sweden (martin.lagging@ medfak.gu.se).

Funding

Received 3 February 2006; accepted 19 May 2006; electronically published 29 August 2006. Presented in part: 12th International Symposium on Hepatitis C Virus and Related Viruses, Montreal, Canada, 2–6 October 2005 (abstract O-07). Potential conflicts of interest: none reported. Financial support: European Community (grant QLK2-2000-00836); Swedish Society against Cancer; Hoffmann–La Roche; Maxim Pharmaceuticals. Reprints or correspondence: Dr. Martin Lagging, Depts. of Virology and Infectious Diseases, Guldhedsgatan 10B, SE-413 46 Göteborg, Sweden (martin.lagging@ medfak.gu.se).

FundersFunder number
La Roche
Maxim Pharmaceuticals
Swedish Society
National Institute of Allergy and Infectious DiseasesR01AI060561
European CommissionQLK2-2000-00836

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