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Influence of Hepatitis G Virus Infection on the Severity of Liver Disease and Response to Interferon-α in Patients with Chronic Hepatitis C

Michele Martinot, MD; Patrick Marcellin, MD; Nathalie Boyer, MD; Jill Detmer, BS; Michele Pouteau, MD; Corinne Castelnau, MD; Claude Degott, MD; Anne Auperin, MD; Mark Collins, PhD; Janice Kolberg, PhD; Judith Wilber, PhD; Jean-Pierre Benhamou, MD; and Serge Erlinger, MD
[+] Article and Author Information

From Hopital Beaujon, Clichy, France; and Chiron Corp., Emeryville, California. Acknowledgments: The authors thank Drs. Francoise Huisse and Jean Paul Bonn (Chiron Diagnostics, Cergy Pontoise, France) for providing the kits. Grant Support: By l'Institut National de la Sante et de la Recherche Medicale (INSERM). Requests for Reprints: Patrick Marcellin, MD, INSERM U24, Hopital Beaujon, 100, Boulevard du Gal-Leclerc, 92118 Clichy, France. Current Author Addresses: Drs. Martinot and Auperin: INSERM U24, Hopital Beaujon, 100, Boulevard du Gal-Leclerc, 92118 Clichy, France.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1997;126(11):874-881. doi:10.7326/0003-4819-126-11-199706010-00004
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Background: Dual infection with hepatitis G virus (HGV) and hepatitis C virus (HCV) is common. The effect of HGV infection on chronic hepatitis C is not well known.

Objective: To assess the prevalence of HGV infection; the effect of HGV infection on the clinical, virologic, and histologic features of patients with chronic hepatitis C treated with interferon-α; and the influence of HGV infection on response to interferon-α therapy.

Design: Retrospective study.

Setting: A university hospital in France.

Patients: 228 patients with chronic hepatitis C treated with interferon-α (3 million U or 5 million U subcutaneously 3 times a week for 3, 6, or 12 months).

Measurements: Before initiation of treatment, serum HGV RNA and serum HCV RNA were detected with branched-DNA assays and HCV genotype was determined with a line probe assay. Serum HGV RNA and serum HCV RNA were detected by polymerase chain reaction at the end of treatment and 6 months after treatment.

Results: Infection with HGV was detected in 21% of patients and 32% of intravenous drug users. The median serum HGV RNA level was 33 × 106 genome equivalents/mL. Infection with HGV was more frequently found in men with a history of intravenous drug use and was associated with HCV genotype 3a (P = 0.02) independent of the source of infection. Serum HCV RNA levels, liver histologic findings, and response to interferon-α therapy did not differ between patients with and those without HGV infection. The loss of serum HGV RNA was not correlated with the biochemical response contrarily to the loss of serum HCV RNA.

Conclusions: Infection with HGV occurred frequently in this sample of patients with chronic hepatitis C, especially in patients infected with HCV genotype 3a. The level of HGV viremia was high relative to the level of HCV viremia. Infection with HGV did not influence the severity of liver disease or response to interferon-α therapy.

Figures

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Figure 1.
Pretreatment serum hepatitis G virus (HGV) RNA levels in 48 patients with chronic hepatitis C and HGV infection (log scale) and serum hepatitis C virus (HCV) RNA levels in 228 patients with chronic hepatitis C virus infection (log scale), according to response to interferon-α therapy.

Each circle represents a patient value; the dashed line represents the cutoff of the assays. For data on median values, see text.

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