title: High baseline interleukine-8 level is an independent risk factor for the achievement of sustained virological response in chronic HCV patients.
abstract: Hepatitis C virus (HCV), a major cause of liver disease throughout the world, is difficult to treat with interferon (IFN) (and various formulations and combinations thereof) being the only approved molecule available. It has been investigated recently that proinflammatory chemokine interleukin-8 (IL-8) induced by HCV partially inhibits the antiviral IFN-α therapy. Therefore, the current study was aimed to prospectively utilize the baseline IL-8 levels in the HCV infected serum and predicts its role in sustained virological response (SVR) to IFN-α+ribavirin therapy, in chronic HCV patients in Pakistan. One hundred and ten hepatitis C patients without any other infections underwent IFN-α+ribavirin combination treatment. Baseline IL-8 levels were determined before starting of the therapy for all these patients. Fifteen normal volunteers negative for HCV were kept as control. The baseline IL-8 levels were found significantly higher in all HCV positive patients as compared to normal healthy volunteers (1083.54 ± 85.72 pg/ml versus 6.99 ± 1.05 pg/ml [mean ± SEM], p<0.01) and were also significantly higher in non-responders than responders (p<0.05). Comparatively higher mean baseline IL-8 levels were observed in non-responders (2442.02 ± 159.92 pg/ml), than late (1009.31 ± 45.31) and rapid (540.91 ± 27.06 pg/ml) responders. Significant relation was observed between baseline IL-8 level and response to IFN therapy (p<0.01). Results of this study suggest that increased levels of IL-8 in HCV infection might be involved in pathogenesis, persistence and resistance to IFN-α+ribavirin combination therapy.
authors.affiliation: National Centre of Excellence in Molecular Biology, University of the Punjab, Lahore, Pakistan. biotech_34@yahoo.com
authors.forename: Haji
authors.initials: H
authors.lastname: Akbar
authors.forename: Muhammad
authors.initials: M
authors.lastname: Idrees
authors.forename: Sadia
authors.initials: S
authors.lastname: Butt
authors.forename: Zunaira
authors.initials: Z
authors.lastname: Awan
authors.forename: Muhammd Farooq
authors.initials: MF
authors.lastname: Sabar
authors.forename: Irshad ur
authors.initials: Iu
authors.lastname: Rehaman
authors.forename: Abrar
authors.initials: A
authors.lastname: Hussain
authors.forename: Sana
authors.initials: S
authors.lastname: Saleem
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D016022:Case-Control Studies; D004359:Drug Therapy, Combination; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000097:blood* / Q000188:drug therapy / Q000276:immunology; D006801:Humans; D007370:Interferon Type I / Q000627:therapeutic use; D016209:Interleukin-8 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010154:Pakistan; D012016:Reference Values; D012254:Ribavirin / Q000627:therapeutic use; D012307:Risk Factors; D017211:Treatment Failure; D019562:Viral Load; D055815:Young Adult
chemical_list: C508606:CXCL8 protein, human; D007370:Interferon Type I; D016209:Interleukin-8; D012254:Ribavirin