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Effect of Hepatitis G Virus Infection on Chronic Hepatitis C

Eiji Tanaka, MD; Harvey J. Alter, MD; Yoshiyuki Nakatsuji, MD; J. Wai-Kuo Shih, PhD; Jungsuh P. Kim, PhD; Akihiro Matsumoto, MD; Masakazu Kobayashi, MD; and Kendo Kiyosawa, MD
[+] Article and Author Information

From Shinshu University School of Medicine, Matsumoto, Nagano-ken, Japan; the National Institutes of Health, Bethesda, Maryland; and Genelabs Technologies, Inc., Redwood City, California. Grant Support: In part by a Grant-in-Aid from the Ministry of Education, Science, Sport and Culture of Japan and a Grant-in-Aid from the Ministry of Health and Welfare of Japan. Requests for Reprints: Harvey J. Alter, MD, Department of Transfusion Medicine, National Institutes of Health, Building 10, Room 1C-711, CC, Bethesda, MD 20852. Current Author Addresses: Drs. Tanaka, Matsumoto, Kobayashi, and Kiyosawa: Second Department of Internal Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Naganoken 390, Japan.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1996;125(9):740-743. doi:10.7326/0003-4819-125-9-199611010-00007
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Objective: To clarify the effect of hepatitis G virus (HGV) infection on chronic hepatitis C.

Design: Retrospective study.

Setting: University hospital in Matsumoto, Japan.

Patients: 189 randomly selected patients with histologically proven chronic hepatitis C, including 101 patients receiving interferon-α.

Measurements: Serum levels of HGV RNA were measured by reverse-transcription polymerase chain reaction. Clinical features, including liver histologic findings, hepatitis C virus (HCV) markers, and response of HCV to interferon-α were compared between HGV RNA-positive and HGV RNA-negative patients.

Results: 21 of 189 (11%) patients with chronic hepatitis C were positive for HGV RNA. On average, patients with HGV RNA were younger than those without HGV RNA (mean age ±SD, 46.6 ± 13.0 years and 51.7 ± 10.7 years, respectively); other demographic and clinical features were similar. The HCV genotype and HCV RNA level were distributed similarly between patients with and those without HGV infection. Ten of 101 patients with chronic hepatitis C who received interferon-α were positive for HGV RNA. The rate of sustained HCV response to interferon-α in patients with HGV infection (30%) was similar to that in patients without HGV infection (36%). The HGV RNA level decreased during therapy in all 9 patients in whom this value was measured. However, only 2 of these patients had a sustained HGV response after discontinuation of therapy.

Conclusions: Patients who only had HCV infection did not differ from patients with HCV and HGV co-infection in clinical presentation, HCV RNA level, or response of HCV to interferon-α therapy. Thus, HGV infection had no apparent influence on the clinical or virologic course of HCV infection. Hepatitis G virus was uniformly sensitive to interferon-α therapy, but only a few patients had a sustained virologic response.

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