OBJECTIVE: A new DNA virus, which has been designated the TT virus, was dis
covered in 1997. It is not clear whether TT virus is a cause of any of the
types of hepatitis. We conducted a case-control study to test the hypothesi
s that the presence of TT virus is a necessary condition for the developmen
t of fulminant hepatic failure in people who have non-A, -B, or -C hepatiti
s.
METHODS: We studied 55 patients with fulminant hepatic failure [28 men, 27
women, mean (+/- SD) age, 47 +/- 15 yr], 32 patients with acute hepatitis (
18 men, 14 women, mean age, 38 +/- 15 yr), and 200 healthy subjects (106 me
n, 94 women, mean age, 42 +/- 14 yr). TT virus DNA was detected in sera by
a nested polymerase chain reaction using a primer set for genotype 1.
RESULTS: TT virus was more frequently detected in patients with fulminant h
epatic failure [in 33 of 55 (60%); 95% confidence interval (CI), 47-73%] th
an in those with acute hepatitis [in 8 of 32 (25%); 95% CI, 10-40%; p = 0.0
016] or in healthy subjects [in 50 of 200 (25%); 95% CI, 19-31%; p < 0.0001
]. TT virus was detected at a significantly higher rate in non-A, -B, or -C
fulminant hepatic failure [in 18 of 22 (82%); 95% CI, 66-98%] than in fulm
inant hepatic failure of A, B, or C type [45%, 28-62%, 15/33; p = 0.007] or
in non-A, -B, or -C acute hepatitis [24%, 3-44%, 4/17; p = 0.0003]. The lo
gistic regression analysis selected TT virus (p = 0.0009), age (p = 0.0116)
, and etiology (p = 0.0309) as independent variables associated with fulmin
ant hepatic failure (coefficient of determination, 0.2335).
CONCLUSIONS: TT virus comparatively plays a role in the pathogenesis of non
-A, -B, or -C fulminant hepatic failure. (C) 2000 by Am. Cell. of Gastroent
erology.