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Does hepatitis GB virus-C infection cause hepatocellular carcinoma in black Africans?
K Lightfoot1, M Skelton, M C Kew
1Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa.
Insights
Hepatitis GB virus-C (HGBV-C) infection does not increase the risk of hepatocellular carcinoma (HCC) in black Africans. Co-infection with HGBV-C also does not elevate HCC risk in individuals with hepatitis B or C virus infections.
Area of Science:
- Hepatology
- Virology
- Oncology
Background:
- Hepatitis GB virus-C (HGBV-C), also known as hepatitis G virus, is globally distributed and causes chronic viremia.
- The pathological role and hepatocarcinogenic potential of HGBV-C remain uncertain.
Purpose of the Study:
- To investigate the association between HGBV-C infection and hepatocellular carcinoma (HCC) in southern African blacks.
- To examine potential interactions between HGBV-C and hepatitis B virus (HBV) or hepatitis C virus (HCV) in HCC development.
Main Methods:
- A case-control study comparing 167 HCC patients and 167 matched controls.
- Detection of HGBV-C RNA using reverse transcription-polymerase chain reaction (RT-PCR) and Southern hybridization.
- Testing for HBV surface antigen, anti-HCV antibodies, and HCV RNA.
Main Results:
- HGBV-C infection was not associated with an increased relative risk of developing HCC (RR 0.9; 95% CI 0.5–1.7).
- HGBV-C co-infection did not increase HCC risk in patients with chronic HBV and/or HCV infections.
Conclusions:
- HGBV-C is not linked to the development of hepatocellular carcinoma in black Africans.
- HGBV-C does not appear to play a role in hepatocarcinogenesis, even in the presence of other hepatitis virus infections.
Abstract:
The newly cloned and characterized hepatitis GB virus-C (HGBV-C), which is the same virus as the independently discovered hepatitis G virus, has a global distribution, is transmitted parenterally, and causes chronic viremia. The pathological consequences of infection with HGBV-C are uncertain, and its hepatocarcinogenic potential is unknown. We used a case-control format to compare the prevalence of HGBV-C infection in 167 southern African blacks with hepatocellular carcinoma (HCC) and 167 race-, age-, and sex-matched hospital-based control subjects, and to test for possible interactive effects between this virus and hepatitis B and C viruses in the development of the tumor. The presence of HGBV-C ribonucleic acid was detected in serum samples by reverse transcription, amplification of the resulting complementary deoxyribonucleic acid by the polymerase chain reaction (PCR), and Southern hybridization using a probe from the NS3/helicase region of the genome. Serum samples were also tested for the presence of hepatitis B virus surface antigen, antibodies to hepatitis C virus, and hepatitis C virus ribonucleic acid. Individuals infected with HGBV-C did not have an increased relative risk of developing HCC (relative risk 0.9; 95% confidence limits 0.5, 1.7). Moreover, co-infection with HGBV-C did not further increase the risk of tumor development in patients who were chronically infected with hepatitis B and/or C viruses. HGBV-C is unrelated to hepatocellular carcinoma development in black Africans.