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; Serge Erlinger, MD
Martinot M, Marcellin P, Boyer N, Detmer J, Pouteau M, Castelnau C, et al. Influence of Hepatitis G Virus Infection on the Severity of Liver Disease and Response to Interferon-α in Patients with Chronic Hepatitis C. Ann Intern Med. 1997;126:874-881. doi: 10.7326/0003-4819-126-11-199706010-00004
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Published: Ann Intern Med. 1997;126(11):874-881.
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.
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.
A university hospital in France.
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).
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.
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.
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.
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