Does hepatitis GB virus‐C infection cause hepatocellular carcinoma in black Africans?

• Published in: Hepatology (Baltimore, Md.) Vol. 26; no. 3; pp. 740 - 742
• Main Authors: Lightfoot, K, Skelton, M, Kew, M C, Yu, M C, Kedda, M, Coppin, A, Hodkinson, J
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.09.1997; Wiley
• Subjects: African Americans; African Continental Ancestry Group; Biological and medical sciences; Carcinoma, Hepatocellular - epidemiology; Carcinoma, Hepatocellular - virology; Case-Control Studies; Confidence Intervals; DNA, Viral - blood; Ethnic Groups; Female; Flaviviridae - isolation & purification; Hepatitis B - complications; Hepatitis C - complications; Hepatitis, Viral, Human - complications; Human viral diseases; Humans; Infectious diseases; Liver Neoplasms - epidemiology; Liver Neoplasms - virology; Male; Medical sciences; Polymerase Chain Reaction; Risk Assessment; Risk Factors; RNA, Viral - blood; South Africa; Tropical medicine; Viral diseases; Viral hepatitis; South Africa; Human; Ethnic origin; Hepatic disease; Hepatocellular carcinoma; Malignant tumor; Epidemiology; African; Infection; Viral hepatitis; Viral disease; Digestive diseases; Complication; Uncertainty relation; Public health
• ISSN: 0270-9139; 1527-3350
• DOI: 10.1002/hep.510260328

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.