GB virus C (hepatitis G) infection

INTRODUCTION

Two viral agents related to hepatitis have been isolated and designated hepatitis G virus (HGV) and GB virus type C (GBV-C). Molecular characterization of these flaviviruses has shown them to be virtually identical isolates of the same virus [1,2]. In comparison, HGV has only 29 percent amino acid homology with HCV [3].

HGV was initially cloned from a surgeon (whose initials were GB, hence the term GB virus or GBV). Plasma from this patient transmitted hepatitis to tamarins. Three different GBV agents were isolated and designed GB virus types A, B, and C; the first two were probably tamarin agents [3]. The agent designated GBV-C is virtually identical to HGV and can be spread by transfusion of contaminated blood and sexual contact, similar to hepatitis C virus and hepatitis B virus [2,4].

DISTRIBUTION

GBV-C has a global distribution, with a high prevalence in the United States donor population. Currently, GBV-C can be diagnosed only by detecting its RNA in the serum by polymerase chain reaction. However, the sensitivity and specificity of this test are not known [3], and one study suggests that it may significantly underestimate the true incidence of infection [5]. In this report, serial serum samples were obtained from 116 injection drug users over a 6.5 year period; a marker of GBV-C infection (either RNA or antibody) was detected in 110, 70 of whom had anti-GBV-C antibodies but were never positive for GBV-C RNA. All eight patients who cleared GBV-C RNA were antibody positive and there were no new infections in 61 antibody-positive subjects. Thus, anti-GBV-C antibodies appear to be highly associated with viral clearance and protection from reinfection.

CLINICAL SIGNIFICANCE OF GBV-C INFECTION

The clinical significance of GBV-C infection with respect to acute or chronic hepatitis is not well understood, but the preponderance of other evidence suggests that GBV-C does not cause hepatitis in humans [6,7].

GBV-C RNA has been detected in patients with acute non-A to non-E viral hepatitis, in patients with chronic hepatitis of presumed viral etiology, in patients with cryptogenic cirrhosis, and in some patients with primary hepatocellular carcinoma. However, it is often difficult to tease out the direct role of GBV-C in these settings since coinfection with HCV is so common. Studies in patients with apparently isolated GBV-C infection suggest that the acute liver injury is similar to and may be less severe than that with HCV [3]. On the other hand, in patients with post-transfusion hepatitis in whom the presence of GBV-C can be documented, the plasma ALT peak and the peak viral titers may be discordant, suggesting that GBV-C may not be responsible for the elevation in ALT levels.