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Hepatitis C Virus Type 1b (II) Infection in France and Italy

Jean-Baptiste Nousbaum, MD; Stanislas Pol, MD, PhD; Bertrand Nalpas, MD, PhD; Paul Landais, MD; Pierre Berthelot, MD, PhD; Christian Brechot, MD, The Collaborative Study Group*
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From Hopital Necker, Institut Pasteur, and Hopital P. Brousse, Paris, France; Jichi Medical School, Tochigi-Ken, Japan; and University of Milan, Milan, Italy. Request for Reprints: Christian Brechot, MD, PhD, Inserm U 370, CHU Necker, 156, rue de Vaugirard, 75015 Paris, France. For a listing of collaborators, see Appendix 2. Grant Support: In part by Institut National de la Sante et de la Recherche Medicale, Pasteur Institute, Diagnostic Pasteur Sanofi, European Community, Association pour la Recherche contre le Cancer, Caisse Nationale d'Assurance Maladie and Fondation pour la Recherche Medicale (JN).

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1995;122(3):161-168. doi:10.7326/0003-4819-122-3-199502010-00001
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Objective: To analyze the distribution of hepatitis C virus (HCV) genotypes among patients positive for antibody to HCV (anti-HCV) according to age, severity of liver disease, and duration of infection; to investigate the influence of HCV genotypes on response to interferon-α therapy; and to study HCV viremia levels in relation to genotypes and severity of liver disease.

Design: Cross-sectional study.

Setting: 3 university hospitals and 2 research units.

Patients: 3 groups of French and Italian patients with chronic HCV infection and detectable serum HCV RNA: Group 1 included 35 patients with hepatocellular carcinoma; group 2, 71 patients with cirrhosis who did not have hepatocellular carcinoma; and group 3, 114 patients with chronic active hepatitis. 106 of the patients with chronic hepatitis or cirrhosis were treated with interferon-α (3 MU subcutaneously 3 times/wk for ≥ 6 months).

Measurements: Genotyping by polymerase chain reaction with capsid-specific primers; serum HCV RNA by branched DNA (bDNA) signal amplification.

Results: Hepatitis C virus genotype 1b (II) was the most prevalent genotype (61.8%). In a univariate analysis, it was associated with older age (<40 years, 47.4%; ≥ 60 years, 80.4%; P = 0.001), longer duration of disease (≤ 10 years, 40.4%; ≥ 20 years, 86.7%; P = 0.005), and cirrhosis with or without hepatocellular carcinoma (78.4% compared with 53.8% for chronic hepatitis; P < 0.001). Viremia levels did not differ between patients infected with HCV type 1b (II) and those infected with other HCV genotypes. Patients with HCV type 1b (II) responded to interferon-α therapy significantly less than did patients with other HCV genotypes (P = 0.01). In a multivariate analysis, age and cirrhosis were independently associated with HCV genotype 1b (II). Genotype and HCV viremia level were independent predictors of response to interferon-α therapy.

Conclusions: The prevalence of HCV genotypes in French and Italian patients has been changing; the prevalence of HCV type 1b (II) infection has progressively decreased, although it still accounts for most HCV-related cirrhosis and hepatocellular carcinoma. High HCV viremia levels and HCV genotype type 1b (II) are independent predictors for poor response to interferon-α therapy and should be considered in the management of patients with HCV infection.

For affiliations and current author addresses, see end of text.*For a listing of collaborators, see Appendix 2.


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Figure 1.
Distribution of the hepatitis C virus genotype 1b (II) in French and Italian patients.Top.Bottom.

The total number of patients for each category is indicated. Distribution according to age. Distribution according to duration of hepatitis C virus infection.

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Figure 2.
Quantitative hepatitis C viremia according to response to interferon-α therapy and 1b (II) or non-1b (II) genotype.5P

The branched DNA (bDNA) assay gives results in numbers of copies of hepatitis C virus (HCV) genome equivalents per mL; results less than the bDNA cutoff but positive by RT-PCR (reverse transcription polymerase chain reaction) are designated as RT-PCR+/bDNA-. Nonresponders to interferon-α therapy had higher levels of HCV viremia than did relapsers or long-term responders (39.1 ± 37.4 compared with 26.5 ± 24.0 × 10 eq genomes/mL; < 0.05).

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