The newly cloned and characterized hepatitis GB virus-C (HGBV-C), whic
h is the same virus as the independently discovered hepatitis G virus,
has a global distribution, is transmitted parenterally, and causes ch
ronic viremia. The pathological consequences of infection with HGBV-C
are uncertain, and its hepatocarcinogenic potential is unknown. We use
d 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 hepat
itis B and C viruses in the development of the tumor. The presence of
HGBV-C ribonucleic acid was detected in serum samples by reverse trans
cription, amplification of the resulting complementary deoxyribonuclei
c acid by the polymerase chain reaction (PCR), and Southern hybridizat
ion using a probe from the NS3/helicase region of the genome. Serum sa
mples were also tested for the presence of hepatitis B virus surface a
ntigen, antibodies to hepatitis C virus, and hepatitis C virus ribonuc
leic acid. Individuals infected with HGBV-C did not have an increased
relative risk of developing HCC (relative risk 0.9; 95% confidence lim
its 0.5, 1.7). Moreover, co-infection with HGBV-C did not further incr
ease the risk of tumor development in patients who were chronically in
fected with hepatitis B and/or C viruses. HGBV-C is unrelated to hepat
ocellular carcinoma development in black Africans.