Following the identification of hepatitis A virus (HAV) and hepatitis B virus (HBV), it was apparent that additional hepatotropic viruses existed. Initially, they were grouped as non-A, non-B hepatitis viruses, and continuing study led to eventual confirmation of hepatitis viruses C, D, and E. However, after these 5 viruses had been described.
Additional cases of hepatitis that were also apparently caused by hepatotropic viruses (sometimes called non-A, non-E viruses) were still occurring.
One putative virus, seemingly found in the stool of patients with clinical hepatitis, was called hepatitis F virus. This virus was not confirmed. Subsequently, an agent called hepatitis G virus was described.
Discovery of Hepatitis G Virus
Hepatitis G virus (HGV) was discovered during the study of patients who appeared to have acute non-A, non-E infection.
Because clinical hepatitis seemed to develop when the virus was present, it was assumed that this was a unique virus. However, subsequent studies failed to confirm HGV as a hepatotropic virus that could result in clinical hepatitis.
In 1966, a surgeon with the initials GB became acutely ill with hepatitis. Samples of his blood were inoculated into marmosets and passed through successive animals, each of which developed evidence of acute hepatitis.
This agent was initially called GB virus (GBV). With subsequent study, 2 viruses were identified (GBV-A and GBV-B), and GBV-B seems to have been the cause of hepatitis in the marmosets.
Virus GBV-C was subsequently isolated from human patients and found to have a structure similar to GBV-A. It was also recognized that the GB viruses were structurally related to hepatitis C virus (HCV).
GBV-C was eventually compared with the agent known as hepatitis G virus, and they were found to be structurally similar, indicating that they were variations of the same virus.
GBV-C was not capable of causing clinical hepatitis in chimpanzees but could do so in marmosets. In chimpanzees, continuing viremia was observed after inoculation, but the animals developed no abnormality in serum aminotransferase levels or changes on biopsy changes indicative of acute hepatitis.
Given the lack of a clear-cut hepatotropic infection of the liver, the use of the term hepatitis G virus seems to be incorrect and has fallen out of favor. The accepted term is now GBV-C, a member of the GBV group.
Epidemiology of GBV-C
GBV-C has a worldwide distribution, and at least 3% of the world’s humans seem to be currently infected. It has been identified in all ethnicities, and 1%- 4% of worldwide blood donors are carriers of the virus at the time of blood donation.
Antibody to virus is even more frequent, and the combined number of persons with viremia and those with antibody suggest that more than 25% of the world population is or has been infected by GVB-C. Most adult patients clear the virus within 2 years of infection.
GBV-C belongs to the Flaviviridae family of viruses, which includes GBV-A, GBV-B, and HCV. GBV-C is an enveloped RNA virus with a single chain RNA structure of positive polarity.
It is composed of approximately 9300 nucleotides with structural genes at the 5′ end, an open reading frame, and nonstructural genes at the 3′ end. It is similar to HCV in structural organization, with approximately 25% homology to HCV in nucleotide sequences.
Multiple GBV-C genotypes have been described,[9,10] distributed as follows:
- Genotype 1 is most common in West Africa;
- Genotype 2 is found in North America;
- Genotype 3 is found in Asia;
- Genotype 4 is found Southeast Asia;
- Genotype 5 is found in South Africa;
- Genotype 6 has been observed in patients from Indonesia.
The site of GBV-C viral replication remains unclear. GBV-C virus is found in low titer in the liver cells in most, but not all, patients, thereby raising the question of its ability to replicate in the liver.
Viral replication definitely seems to occur in mononuclear cells, including CD4 and CD8 T cells and B cells.
- Hepatitis G Virus (HGV). Also known as GB virus-C (GBV-C)
- HGV and GB virus-C were discovered about the same time, and are thought to be different strains of the same virus. Referred to below as HGV/GBV-C.
- HGV/GBV-C was first described in 1995-96
- HGV/GBV-C is a single stranded RNA virus belonging to the Flaviviridae family
- Carrier rate of between 2 and 5% in the general population.
- Causes persistent infection for up to 9 years in 15-30% of adults.
- HGV/GBV-C is often found in co-infections with other viruses, such as hepatitis C virus (HCV), hepatitis B virus (HBV), and Human Immunodeficiency Virus (HIV)
- There is little proof that Hepatitis G (Hep G) causes serious liver disease at any age. It is possible that
- HGV/GBV-C may not be a true ‘hepatitis’ virus.
Signs and Symptoms
Almost no cases have symptoms like the other Hepatitis viruses.
Modes of Transmission
Transmitted by infected blood or blood products
HGV/GBV-C can be transmitted by sharing personal items contaminated with the virus and other similar behaviours (parenterally), from mother-to-newborn child at birth (vertical), or various sexual activities.
Persons at Risk
- Persons Level of Risk Recipients of infected blood or blood products
- Hemodialysis patients
- Injection Drug Users
- People getting tattoos, acupuncture or body piercings with tools that are not sterile
- People with impaired immune response
- People who engage in prostitution
If you are regularly exposed to blood or blood products from others, try to protect yourself with gloves to reduce the risk of the spread of viruses.
If you use injection drugs, ensure you use clean, sterile needles. Sharing needles, syringes or other drug-use equipment with others can put you at risk of infection.
There is currently no recommended treatment for Hep G.
Diagnosis of GBV-C
GBV-C RNA can be identified in the blood of infected individuals by use of reverse transcriptase polymerase chain reaction. According to this technique, viral particles are present in liver cells, endothelial cells, monocytes, and lymphocytes.
With clearance of infection, antibody to the envelope glycoprotein E2 develops and may be recovered from the serum. Most patients will develop detectable anti-E2 antibody after clearance of the virus. Coexistence of circulating GBV-C virus and anti-E2 antibody is infrequent, occurring in less than 5% of patients.