J Am Soc Nephrol 10: 1828 –1832, 1999
SCIENCE WATCH
TT Virus
PETER A. L. BONIS
UpToDate, Inc. Wellesley, Massachusetts, and New England Medical Center, Boston, Massachusetts.
Abstract. TT virus (TTV) is a newly described DNA virus that
was first detected in the blood of three patients with elevated
serum aminotransferases following transfusion who tested neg-
atively for all known hepatitis viruses. The virus has been
After the discovery of the hepatitis A and B viruses in the
1960s and 1970s, it became apparent that an unidentified agent
was responsible for hepatitis in a number of patients suspected
of having acute or chronic viral hepatitis. The unknown patho-
gen was referred to as non-A non-B hepatitis until the hepatitis
C virus was identified in 1989 and was found to account for
hepatitis in the majority of these patients (1).
However, in approximately 5% of patients with liver dis-
ease, no cause can be identified (2). It has long been suspected
that additional hepatotropic viruses will be discovered to ac-
count for some of these cases, especially since approximately
half of these patients have a history of blood transfusion (2).
The hepatitis G virus, identified in 1996, has proven to be an
unlikely candidate since an association with hepatitis or any
other disease has not been consistently demonstrated (3).
A novel virus associated with posttransfusion hepatitis was
identified in 1997 in three patients from Japan who developed
elevated serum aminotransferase concentrations following
transfusion and tested negatively for all known hepatitis vi-
ruses (4). The virus (referred to as TT virus for the initials of
the patient in whom it was isolated or “transfusion transmitted
virus” [TTV]) exhibited hepatotropism, and its titers correlated
with elevation in serum aminotransferase concentrations sug-
gesting that it was a true hepatitis virus.
Accumulating data have demonstrated a high prevalence of
the virus in the general population, demonstrating that it is
capable of producing chronic infection. TTV DNA has been
detected in approximately 2% of blood donors in the United
Kingdom, 1 to 10% in the United States (5,6), 12 to 40% in
Japan (7–9), 14% in Korea (10), 13% in Germany (11), 62% in
Brazil (12), 11% in Spain (13), and 10% in Columbia (14).
TTV may be acquired early in life, particularly in countries
with a high prevalence of infection in the general population. A
series from Japan found that 5% of 197 children seen in a
general pediatric center had TTV DNA detectable in serum
Correspondence to Dr. Peter A. L. Bonis, UpToDate, Inc., 34 Washington
Street, Wellesley, MA 02481. Phone: 781-235-3065, extension 288; Fax:
781-239-0391; E-mail: Pbonis@UpToDateInc.com
1046-6673/1008-1828
Journal of the American Society of Nephrology
Copyright © 1999 by the American Society of Nephrology
found worldwide with a high prevalence in the general popu-
lation. However, accumulating evidence suggests that the virus
is not a significant cause of acute or chronic liver disease. No
other disease associations with infection have been described.
(15). In another report from the Democratic Republic of
Congo, TTV was found in 61 of 105 women (58%) attending
an antenatal clinic and 36 of 68 (54%) of infants (16). The
virus can be detected in the stool and bile of infected patients,
suggesting that it may be transmitted enterally (17,18).
A high prevalence of infection has been found in patients
with parenteral exposure to blood. TTV DNA was detected in
44% of patients with hemophilia in the United Kingdom (19),
and up to 75% in Japan (20,21). A report from China found a
prevalence of 22% among those with a history of intravenous
drug use. (22). TTV was present in 84% of Italian patients with
transfusion-dependent beta thalassemia (23).
Despite its high prevalence, an association between TTV
infection and acute or chronic hepatitis or other diseases has
not been consistently observed. Furthermore, the initial obser-
vation of hepatotropism has not been confirmed (24), and
injection of the virus into chimpanzees, while capable of caus-
ing infection, did not produce clinical illness (25).
Phylogenetic Analysis
TTV is an unenveloped, single-stranded DNA virus that has
similarities to the Circoviridae viruses known to infect plants
and vertebrates (25). However, it has been classified as a
member of a new family of viruses, the Circinoviridae, based
on its distinct biophysical and molecular characteristics.
Phylogenetic analysis of isolates pooled from worldwide
sources has demonstrated at least three genotypes and multiple
subtypes (designated 1a, 1b, 1c, 2a–f,and 3); the different
genotypes do not appear to be geographically clustered (21,25–
33). A possible fourth genotype has been reported in Columbia,
Belgium, and Korea (10,14,31).
The majority of patients are infected by genotype 1. How-
ever, coinfection with multiple genotypes is common, partic-
ularly in patients who have had multiple exposures to blood
products (28). No differences in clinical outcomes among the
various genotypes have been observed (32).
Natural History
The natural history of TTV infection has not yet been
defined. The presence of TTV infection has been based on the
detection of its DNA in serum or tissue samples. Thus, little is
known about the immune response to the virus or the frequency
J Am Soc Nephrol 10: 1828 –1832, 1999
with which an acute exposure leads to viral clearance. Anti-
bodies against TTV have been detected and will help to clarify
these issues (34).
Preliminary reports in patients who have been followed
longitudinally have suggested a low rate of viral clearance. As
an example, TTV DNA remained persistently detectable for 3
yr in a cohort of 19 patients (35). In another report, 97% of 93
patients who were followed for 3 yr remained viremic (23). A
third series suggested an annual clearance rate of approxi-
mately 7% (36). However, many of the patients in these series
had exposure to blood products. Thus, the extent to which the
persistence of TTV DNA represents chronic infection by a
single genotype or the acquisition of new genotypes remains
uncertain.
Clinical Significance
The presence of TTV has been sought in a number of clinical
settings, which will be summarized below. However, much of
the information has been reported only in preliminary form.
Thus, an understanding of its possible clinical significance is
evolving.
Hemodialysis
A number of series have found a high prevalence of TTV
infection among patients undergoing hemodialysis particularly
in Japan (30,36 –39). As an example, in a series of 115 patients
from Japan, TTV DNA was detected in 51%, compared to 13%
in healthy blood donors (37). Serum alanine aminotransferase
concentrations were similar between those with and without
TTV DNA.
The high prevalence among Japanese patients on hemodial-
ysis may reflect the relatively high prevalence in the general
population. A much lower prevalence of infection was found in
a series from France in which TTV DNA was detected in only
two of 84 (2%) patients on hemodialysis (40). In addition, the
prevalence of TTV infection may depend on the number of
years that patients have been receiving hemodialysis (38). This
was illustrated in a series that included 50 Japanese patients
with hepatitis C who were followed for 48 mo while on
hemodialysis (36). TTV DNA was present in 48% at the start
of the study. A history of blood transfusions was similar among
those with and without infection. During follow-up, four pa-
tients developed new infection; the estimated annual infection
rate was 4%. However, in other reports, the presence of TTV
was unrelated to the number of years of dialysis (39).
Renal Transplantation
A study from Japan found that the acquisition of TTV
infection after renal transplantation was common but of uncer-
tain clinical significance (39). New infection after transplanta-
tion was detected in nine of 25 (36%) patients. Three of these
patients demonstrated an elevated serum alanine aminotrans-
ferase concentration, which subsequently normalized in two.
An adverse effect on graft survival has not been reported.
TT Virus 1829
Association with Acute Liver Disease
TTV DNA has been detected in patients with acute hepatitis
of otherwise unknown etiology (7,8,41– 44), but a correlation
of TTV titers and serum aminotransferase concentrations has
been inconsistent. Thus, it remains unclear whether the virus
was the cause of the liver disease or was an incidental finding.
Some reports have suggested that the virus may be associ-
ated with acute hepatitis in a subset of patients. This was
illustrated in a study that included 25 Japanese patients under-
going bone marrow transplantation of whom 60% were posi-
tive for TTV DNA after transplantation (45). No significant
difference was observed in the incidence of veno-occlusive
disease, graft versus host disease, or biochemical evidence of
liver dysfunction based on TTV status. However, in one patient
serial semiquantification of TTV DNA in serum closely cor-
related with the serum alanine aminotransferase levels. A liver
biopsy specimen was consistent with acute hepatitis, and TTV
DNA was detectable in liver tissue by PCR.
Association with Chronic Liver Disease of
Unknown Etiology
The presence of TTV DNA does not appear to be associated
with biochemical or histologic evidence of liver injury of
unknown cause in most reports (24,40,46 – 48). In one study,
for example, no significant difference in the prevalence of TTV
DNA was found between 99 blood donors in the United States
who had an elevated serum alanine aminotransferase compared
with 46 control subjects (46). Similar findings were found in
Spain (13). In a report from Japan, the prevalence of TTV
DNA was similar between 50 patients with chronic liver dis-
ease of unknown etiology and 106 volunteer blood donors (47).
In contrast to these reports, another series from Japan sup-
ported a potential role for TTV in the development of chronic
liver disease (42). The prevalence of TTV DNA was signifi-
cantly higher among 57 patients with chronic liver disease of
unknown etiology compared to 96 patients known to have
chronic liver disease due to hepatitis C (47% versus 18%).
Similarly, in a series from the United States, the prevalence of
TTV was much higher among 33 patients with cryptogenic
cirrhosis compared with 100 healthy blood donors (15% versus
1%) (5).
Association with Known Forms of Chronic
Liver Disease
Several reports have demonstrated an increased prevalence
of TTV DNA in patients with a variety of chronic liver diseases
compared to control populations (5,20,21,49 –51). As an ex-
ample, in one series from the United States, TTV was present
in 27% of patients with fulminant hepatic failure and 18% of
cirrhotic patients with a history of blood transfusion compared
to 1% in healthy blood donors (5). However, in most reports
TTV does not appear to contribute to the liver injury. In a study
from Japan, for example, TTV DNA was not more common
among hemophiliacs with an elevated alanine aminotransferase
who were infected by hepatitis C virus compared to hepatitis C
1830 Journal of the American Society of Nephrology
virus-negative control subjects, suggesting that the liver injury
was due to hepatitis C virus alone (21).
In another report from the United Kingdom, the prevalence
of TTV DNA among patients with chronic liver disease was
similar to healthy control subjects (52). No significant differ-
ence was noted in the rate of TTV DNA among various forms
of liver disease. The majority of TTV-positive patients had no
biochemical or histologic evidence of significant liver disease.
Thus, the increased prevalence of TTV among patients with
various forms of liver disease suggests shared risk factors with
TTV infection.
Similar results have been found in other centers, which have
also not detected a correlation between TTV status and the
severity of liver disease (9,19,35,53,54) or outcome in patients
undergoing treatment of hepatitis C virus with interferon
(9,36,48,55). Interferon treatment has been associated with
clearance of TTV infection.
TTV DNA has been sought in a number of other settings
related to liver disease. It does not appear to serve as a trigger
for autoimmune hepatitis (56,57). No association between TTV
DNA and cryoglobulinemia was found in a single report (58).
Liver Transplantation
TTV is frequently acquired after liver transplantation pre-
sumably because of the multiple transfusions that are often
required during the procedure. In one report from the United
States, for example, TTV DNA was found after transplantation
in up to 44% of those who were initially negative for the virus
before the procedure (59).
Despite its high prevalence, its significance in the transplant
setting is uncertain. In one report, patients who were TTV-
positive after transplantation were significantly more likely to
have idiopathic hepatitis on protocol liver biopsies at 12 mo
(60). However, in other series TTV did not appear to have any
association with clinical or histologic evidence of hepatitis
(48,61).
Conclusion
An understanding of the biology and clinical significance of
TTV is evolving. Increasing evidence suggests that it is not a
significant cause of liver disease, although it may be capable of
inducing hepatitis in a subset of patients. The continued search
for TTV in non-liver-related clinical settings will help to de-
termine whether the virus contributes to other human diseases.
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