GB Virus C (GBV-C) - Hepatitis G Virus

Andi Cahyadi

History

            In 1967, from a surgeon with the initials GB who suffered from acute hepatitis, GB virus can be isolated and the experiments successfully transmitted to the tamarin monkey (Masuko et al., 1996). Then two new virus can be isolated which is a positive strand RNA viruses including Flaviviridae family, namely GB virus type A (GBV-A) and GB virus type B (GBV-B) (Simons et al., 19 951). It turned out that GBV-A and GBV-B is only found in the tamarin monkey (Alter et al, 1996).

            Leary et al. in 1996 found another virus that GBV-C in patients with acute hepatitis, chronic and healthy people who live in the United States, Canada and Africa. GBV-C is found in people with risk of exposure to viral hepatitis, including exposure to non-AE viral hepatitis (Alter et al, 1996). In the same year successfully isolated a new virus called hepatitis G virus (VHG) from patients with chronic hepatitis in the United States (Linnen et al., 19 961). GB virus C (GBV-C) and Hepatitis G Virus (HGV) is a fairly new virus in humans, which was found by two different research groups. Both the virus was identified from patients with hepatitis caused by viruses. As well as the Hepatitis C virus (HCV), VHG and GBV-C has the same amino acids and nucleotides more than 95% and 85%, so the second concluded the virus originated from the same virus species with different isolates (Retno et al., 2000 .) For further discussion both virus called GBV-C.

The structure of GBV-C

GBV-C including the family Flaviviridae, which consists of single stranded RNA molecules and has approximately 9500 nucleotides (Sherlock, 1999). Twenty-five percent of GBV-C has the same amino acid with HCV, and the nature kronisitasnya quite prominent in human infection. Genome as a whole pattern similar to VHC and other Flavivirus (In Bisceglie, 1996). This virus is unique among Flafiviridae because it does not encode a protein that resembles the core (core like protein) which is a protein that is located near the amino end of poliprotein virus.

Complete genome sequence of the isolated HGV and GBV-C has now been determined. Both are positive strand RNA virus which in fact has almost the same nucleotide sequence. HGV amino acids and GBV-C has a 29% homology with HCV, which indicates that the virus is different and not the serotypes of HCV. HGV and GBV-C has the amino acid homology of 48% with GBV-A and 28% with GBV-B. In the conversations that HGV and GBV-C will be referred to as GBV-C. GBV-C has two kinds of protein that is 2 structural proteins (E1 and E2 proteins) and 5 non-structural proteins (proteins NS2, NS3, NS4, NS5A and NS5B) (Tillmann et al., 2001) (Figure 1). E2 protein is a key protein that can stimulate the formation of antigen in the body.

GBV-C can be bred (inoculated) into the body of primates such as chimpanzees, and macaques tamarin. Also, studies Tan et al. (2002) showed that this virus can be duplicated in vitro by inoculation into the PBMCs (Peripheral Blood mononuclear cell). This is a good omen that in the future pengembangbiakkkan GBV-C is feasible.

  
Prevalence and GBV-C Transmission Line

GBV-C can be transmitted through blood and blood products, sexual contact, and vertically from mother to fetus. GBV-C also can be transmitted through infected serum in animal primates, including the tamarin, chimpanzee and macaque monkeys. GBV-C was detected in many drug users of intravenous drugs. The prevalence of GBV-C differ in various populations. Centers for Disease Control and Prevention has found among patients in the United States are diagnosed with hepatitis non-A, non-B of approximately 18% are positive GBV-C RNA in which the majority of patients (80%) were also infected with HCV (DiBisceglie, 1996; CDCP, 1996),

GBV-C infection can occur in healthy blood donors (Linnen et al., 19 962). The prevalence of GBV-C infection in blood donors in Surabaya, Indonesia at 2.7%. While the prevalence of GBV-C infection and coinfection with HCV that occurs in patients with chronic liver disease in Surabaya by 8.4% (Retno et al., 2000).

GBV-C infection is found widely in the world and easily transmitted by transfusion or other parenteral route. Because GBV-C infection is mainly through the parenteral route, then the patients who are undergoing hemodialysis have a high risk to be infected with GBV-C (Linnen et al., 19 961). About 3% of kidney dialysis patients have GBV-C RNA in their blood (Masuko et al., 1996) but other researchers found a higher prevalence (Tanaka et al., 1996).

High risk groups in the transmission of GBV-C is the commercial sex workers and homosexual men. In Taipei, Taiwan, 21% female commercial sex workers without a history of intravenous drug use found GBV-C RNA positive. Seroprevalence of GBV-C RNA in a positive homosexual men infected with HIV in Frankfurt, Germany, was 8.5%. The same researchers analyzed the antibodies against the envelope glycoprotein E2 (E2Ab) of GBV-C and found the prevalence overall of 31.9%. In Spain, the prevalence of GBV-C RNA has been reported by 13.4% and 19%. 51% of HIV-infected homosexual men in Scotland showed GBV-C RNA positive and 4 of the 17 negative samples, the PCR became positive. Transmission through sexual contact plays an important role in the development of a relatively new biological viruses found this. History of sexually transmitted diseases was significantly associated with GBV-C infection before (Wacthler et al., 2000).

Diagnosis of GBV-C

Specific diagnosis according to type of virus that causes can only be determined through laboratory examination (Hardie, 2005). Diagnosis of infection with GBV-C is done by examination of Polymerase Chain Reaction (PCR) is to detect viral RNA in serum, tissue or other infected fluid. PCR is still the superior method available today for diagnosis of infection with GBV-C. Possible mismatch PCR test results with the prevalence of GBV-C infection can occur in people who have recovered from infection or at the time did not contain GBV-C again (In Bisceglie, 1996).

Clinical Aspects of Infection with GBV-C On The Body

Unresolved issue is whether GBV-C cause hepatitis or other diseases. Because infection with GBV-C and HCV is associated then it becomes difficult to analyze the effect of GBV-C itself. Among patients with GBV-C infection that developed into hepatitis, liver damage is not severe and often appear lighter than HCV infection alone (Tanaka et al., 1996).

Tanaka (1996) examined 189 patients who had symptoms such as chronic hepatitis C and found 21 people (11%) carrying GBV-C RNA in serum. However, less than 20% of patients with cirrhosis cryptogenik or other forms of chronic hepatitis of unknown cause was also infected with GBV-C. Determination of GBV-C is still difficult because of the chronic course of illness largely GBV-C along with another hepatitis virus infection. Thomas et al. (1997) showed that GBV-C only as an innocent bystander virus (the virus that are not influential broadcaster.) This can be proved through the examination of histology and biochemistry of people with GBV-C positive and GBV-C negative. In both groups found no significant difference in liver histology and serum transaminase enzyme elevations. It also found significant differences in GBV-C infection of immunocompetent people and imunokompromise (Pessoa et al., 1998).

Since wearing serologic HBsAg and anti-HCV as a filter for blood donors, the incidence of post-transfusion hepatitis declined rapidly. But examination screened for HBsAg and anti-HCV does not reduce the risk of infection with GBV-C, although it showed some blood recipients had been infected with HCV and GBV-C before transfusion done, so need to test strain of GBV-C alone (Tillman et al., 2001) .

There are unique clinical course of GBV-C infection. With a mechanism that remains unknown, GBV-C could be free of the immune response in the human body. There is evidence to support this statement: First, GBV-C could survive long in the human body to more than 10 years. Second, during GBV-C RNA positive, in human blood can not find the presence of antibodies against GBV-C E2 protein. Vice versa when a person recovers from infection with GBV-C (not found GBV-C RNA in the blood) appear before antibodies to the E2 protein. Third, GBV-C merupkan low density particle that has a low immunogenic power.

Management of acute GBV-C together with other acute viral hepatitis, ie a total break with a diet low in fat and high in protein and enough calories. Provision of interferon (IFN) of 5 million units every day or 10 million units 3 times a week for at least 6 months to suppress replication of GBV-C, but almost all cases of relapse after IFN α discontinued (Karayiannis et al., 1997). Given that little research is currently ongoing and still being a few studies on GBV-C, then a rational pharmacotherapy recommendations for GBV-C has not been issued. (Nurjanah, 2001). Hepatoprotector preparations (such as schizadrine, curcuma, Fructus, ginseng) can be used on GBV-C infection because it has a working cell and protection against liver function

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