Ld. Moaven et al., HEPATITIS-G VIRUS AND FULMINANT HEPATIC-FAILURE - EVIDENCE FOR TRANSFUSION-RELATED INFECTION, Journal of hepatology, 27(4), 1997, pp. 613-619
Background/Aims: In the majority of cases of fulminant ''viral'' hepat
itis in Australia, no known aetiological agent can be isolated, We hav
e examined the possible role of the recently discovered hepatitis G vi
rus (HGV) in such cases.Methods: An HGV specific reverse transcription
polymerase chain reaction (RT-PCR) was performed on pre- and post-liv
er transplant serum from 14 patients who were referred for transplanta
tion at our unit between 1989 and 1995 for unexplained fulminant hepat
ic failure, Eleven patients successfully underwent transplantation and
three died while waiting for a suitable donor organ, Hepatitis viruse
s A-E were excluded by standard serological and PCR based testing, HGV
RT-PCR was also performed on 21 other, randomly selected, liver trans
plant recipients (''controls''). Results: The 14 fulminant cases were
HGV RT-PCR negative prior to transplantation while five of 21 controls
were positive, Post-transplant, eight of the 11 fulminant patients we
re found to be HGV RT-PCR positive and the same five controls remained
HGV RT-PCR positive, In three of the eight fulminant patients the HGV
infection resolved. Conclusions: Our data indicate that HGV infection
is unlikely to be responsible for fulminant hepatitis and that it is
probably acquired from blood and/or blood products during the transpla
ntation process, Furthermore, long-term carriage of HGV post-transplan
t is not associated with clinically apparent liver disease.