Viral hepatitis is known to be caused by at least five distinct viruses (A, B, C, D and E) that can result in acute infection. Hepatitis B, C and D viruses can result in chronic infection. A novel agent called hepatitis F has been described but has not yet been confirmed. Another hepatitis virus, the hepatitis G virus, has been identified, confirmed and cloned. Hepatitis G virus has been reported to be associated with other diseases such as aplastic anemia. Cheung and colleagues reviewed the literature to examine the association between hepatitis G virus and various liver diseases.

Hepatitis G is an RNA virus similar to other viruses in the Flaviviridae family. Currently, serologic testing for hepatitis G is not available. Hepatitis G virus infection can only be diagnosed by polymerase chain reaction assay, which detects viral RNA in serum. Hepatitis G antibody assays to detect evidence of past infection are not available. An enzyme-linked immunosorbent assay for detection of antibodies has recently been described as a potent serologic marker for immunity to hepatitis G virus infection, but further studies are needed.

Studies indicate that the prevalence of hepatitis G virus among blood donors ranges from 0.9 to 10.0 percent. The prevalence among populations receiving multiple blood products has been found to be 5.4 to 18.6 percent among patients with hemophilia and 18.0 percent among anemic patients requiring multiple transfusions. Hepatitis G virus is a blood-borne virus that is parenterally transmitted. However, as in hepatitis C, many patients who are positive for hepatitis G have no identifiable parenteral risk factors.

The role of hepatitis G virus in post-transfusion hepatitis is uncertain. The correlation between the presence of the virus and chronic liver disease is poor. Hepatitis G is rarely a cause of post-transfusion hepatitis.

Some evidence indicates that hepatitis G virus is a causative factor in acute community-acquired non-A–E hepatitis, but hepatitis G is not a major cause of acute community-acquired hepatitis in the United States. Most cases of hepatitis G virus infection occur in the setting of coinfection with other hepatitis viruses, such as hepatitis B and C. Hepatitis G virus seems to have little effect on the course of infection or the response to interferon therapy, and the clinical course is largely determined by the coinfecting virus.

The role of hepatitis G virus in hepatocellular carcinoma is unclear. Serum hepatitis G RNA, usually along with hepatitis B or C, has been found in patients with hepatocellular carcinoma. In an Austrian study, hepatitis G RNA was the only infectious viral agent identified in 8 percent of 85 patients with hepato-cellular carcinoma. It is believed that hepatitis G is unlikely to be a major etiologic agent in hepatocellular carcinoma.

No data exist on the treatment of patients with hepatitis G virus alone, since the role of hepatitis G in chronic viral hepatitis has not yet been determined. Treatment response in patients coinfected with hepatitis G virus and another hepatitis virus is similar to that of the other hepatitis virus.

The authors conclude that although hepatitis G virus appears to be a hepatotrophic virus, its independent role in acute and chronic liver disease is unclear. Correlation is poor between serum hepatitis G RNA and elevation of alanine transaminase levels, and viremia frequently occurs without alanine transaminase elevation. Therapy for hepatitis G virus is not yet recommended, since its role as an etiologic agent in liver disease is unclear. Interferon could be used if hepatitis G virus infection were to be demonstrated as a cause of liver disease.

In a related editorial, Bonkovsky points out that the most striking association to cause concern is between hepatitis G virus and aplastic anemia following acute hepatitis, although even this relationship requires further substantiation. He states that the type and severity of hepatitis that hepatitis G virus might cause is so minor as to put doubt on the categorization of this virus as a hepatitis virus.