Non-A, non-B hepatitis viruses have been implicated as the etiological
agent(s) in up to 60% of patients with fulminant hepatitis. These age
nts are reported to induce a higher mortality than other causes of ful
minant hepatitis. Hepatitis E virus (HEV) and hepatitis C virus (HCV)
at present constitute the major identifiable non-A, non-B hepatitis ag
ents. Of these, HEV has been established as the sole cause of epidemic
hepatitis in Afro-Asian countries, and fulminant hepatitis has been r
ecorded during such epidemics. However, in sporadic cases, the etiolog
ical role of HEV in fulminant hepatitis has remained uncertain. The ro
le of HCV in acute liver disease and fulminant hepatitis remains uncle
ar. The present study was undertaken to investigate the association of
HEV and HCV in patients with fulminant hepatitis by direct detection
of the viral genome using reverse transcription-polymerase chain react
ion (RT-PCR). Serum samples from 50 serelogically identified non-A, no
n-B fulminant hepatitis cases negative for cryptic hepatitis B virus (
HBV) infection examined via PCR were tested for HEV and HCV RNA using
RT-PCR. For HEV primers from the nonstructural region (ORF-1) were use
d, and for HCV primers from the highly conserved 5' untranslated regio
ns were used. The products were analysed using agarose gel electrophor
esis and confirmed by hybridisation with radiolabelled internal oligon
ucleotide probes. HEV was detected in 31 (62%) of the 50 fulminant non
-A, non-B hepatitis cases. In 18 (36%) cases, HCV RNA was detected. In
11 (22%) of the HCV cases, the HEV genome was also amplified. In 20 (
40%) cases, HEV was detected alone. Twelve (24%) patients were negativ
e for all viral hepatitis markers. This study establishes HEV as one o
f the major agents associated with sporadic fulminant hepatitis in a g
eographical region where epidemics of hepatitis caused by HEV are freq
uent. (C) 1994 Wiley-Liss, Inc.