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Canadian Journal of Gastroenterology
Volume 13, Issue 10, Pages 814-818
Original Article

GB Virus C Infection: Clinical Significance

Xiang Wei Meng,1 Masafumi Komatsu,1 Shigetoshi Ohshima,1 Kunio Nakane,1 Tomoo Fujii,1 Takashi Goto,1 Kazuo Yoneyama,1 Tomoyuki Kuramitsu,1 and Motokazu Mukaide2

1First Department of Internal Medicine, Akita University School of Medicine, 1-1-1 Hondo, Akita City, Japan
2Center for Molecular Biology and Cytogenetics, SRL Inc, Tokyo, Japan

Received 13 December 1997; Accepted 11 November 1998

Copyright © 1999 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


GB virus C (GBV-C) RNA positivity rates were examined in serum specimens from 231 patients with liver disease (23 patients with hepatitis B, 175 patients with hepatitis C, five patients with hepatitis B virus plus hepatitis C virus coinfection, and 28 patients with non-A, non-B, non-C hepatitis) to clarify the clinical significance of this virus. GBV-C RNA was detected in none of 12 patients with fulminant hepatitis, one of two patients with acute hepatitis positive for hepatitis B surface antigen and one of four patients with acute non-A, non-B, non-C hepatitis. Pathogenetic involvement of GBV-C was suspected in some patients in the latter group. Among patients with the non-B, non-C type of chronic disease, one of seven with cirrhosis (14%) and none with chronic hepatitis or hepatocellular carcinoma were GBV-C-positive. In chronic hepatitis C patients who had received interferon treatment, no difference was found in clinical findings, alanine aminotransferase (ALT) concentrations, histology or response to interferon between 11 patients who were GBV-C RNA-positive and 101 patients who were GBV-C RNA-negative. Moreover, changes in ALT after interferon therapy showed no relation to positivity for GBV-C RNA. On the basis of these findings, GBV-C appears to be an unlikely cause of initiation or progression of chronic hepatic diseases.