GB Virus C/Hepatitis G Virus

Abstract

Hepatitis G virus (HGV) is a positive, single-strand RNA virus that has been classified in the family Flaviviridae. The 5′-untranslated region (UTR) of the HGV genome is lengthy and does not share any significant primary and secondary RNA structures with the 5′-UTR of hepatitis C virus (HCV). The internal ribosome entry site has extraordinarily weak activity. The HGV genome does not seem to encode a nucleocapside protein analogous to HCV. Blood-borne transmission is presumed to be the commonest mode of transmission of the virus. Current infection with HGV is diagnosed by detection of HGV RNA by the polymerase chain reaction (PCR), and past infection with HGV is detectable by testing anti-HGV E2. HGV is distributed worldwide, but its prevalence varies widely from one population to another. Although the prevalence of HGV in association with acute and chronic hepatitis is higher than that in the general population, further prospective studies are needed to demonstrate its relative significance in causing hepatitis and other disease. The major unresolved biological issue at the moment is its hepatotropsim and site of propagation. Recent progress demonstrates that HGV replicates in lymphocytes rather than hepatocytes. HGV may be pathogenic under special conditions, but does not influence carcinogenesis.

Full-Length GB Virus C (Hepatitis G Virus) RNA Transcripts Are Infectious in Primary CD4-Positive T Cells

“…Characterization of PBMC subsets identified the CD4 ϩ T cells as the cells supporting GBV-C replication. Although early studies suggested that GBV-C replicates in the liver, most reported studies indicate that GBV-C is not hepatotropic (20,24). Our inability to demonstrate infection of HepG2 cells is consistent with this, although we were also unable to demonstrate persistent replication in the CD4 ϩ T-cell line (MOLT-4).…”

GB Virus C epidemiology in denmark: Different routes of transmission in children and low‐ and high‐risk adults

“…In contrast, it has been shown lately that HIV patients co-infected with GBV-C have a lower mortality than other HIV-infected patients [Tillmann et al, 2001;Xiang et al, 2001]. The virus replicates in haemapoetic cells but apparently not in hepatocytes, and we will refer to the virus as GBV-C in this paper [Kiyosawa and Tanaka, 1999;Xiang et al, 2001;Tucker and Smuts, 2001].…”

Effect of HGV-infection on clinical course of hepatitis C and the possible role of endogenous interferon

“…It is shown that co-infection HGV with HBV aggravates the defeat a liver affection, whereas in combination with HIVinfection have a beneficial effect on its clinical current (Chams et al, 2003;Lau et al, 1999;Muerhoff, Tillmann et al, 2003). According to some data HGV does not influence on the other hepatitis development (Enomoto, Shuhei et al, 1998;Kiyosawa and Tanaka, 1999). At the same time another group of Japanese researchers showed that current of hepatitis C in combination with HGV-infection has a mild form (Tanaka, Alter et al 1996;Karayiannis, Hadziannis et al, 1997).…”