Hepatic disorders are a frequent complication in patients with hematologic diseases,
who often require transfusions of blood products. Posttransfusion hepatitis is a problem
in these patients, despite screening for hepatitis B and C viruses. Hepatitis G virus
was discovered as a transfusion-transmissible flavivirus in 1996 (
1
). Subsequently, however, it was shown that this virus rarely causes hepatitis, even
in immunosuppressed patients (
2
,
3
). Recently, a novel DNA virus, named TT virus, was cloned from serum of a patient
with posttransfusion hepatitis (
4
). TT-virus DNA was detected in serum samples from three of five patients with posttransfusion
non–A to G hepatitis. The serum TT-virus titer closely correlated with the serum alanine
aminotransferase level (
4
). Thus, it may be a potential causative agent for non–A to G hepatitis. In this study,
we investigated the prevalence and clinical effects of TT virus in frequently transfused
patients with hematologic diseases.To read this article in full you will need to make a payment
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References
- Molecular cloning and disease association of hepatitis G virus.Science. 1996; 271: 505-508
- Hepatitis G virus—a true hepatitis or an accidental tourist?.NEJM. 1997; 336: 795-796
- Quantitation of hepatitis G virus RNA in bone marrow transplant recipients.Br J Haematol. 1998; 100: 798-800
- A novel DNA virus (TTV) associated with elevated transaminase levels in posttransfusion hepatitis of unknown etiology.Biochem Biophys Res Commun. 1997; 241: 92-97
- Molecular cloning and characterization of a novel DNA virus (TTV) associated with posttransfusion hepatitis of unknown etiology.Hepatol Res. 1998; 10: 1-16
Article info
Publication history
Published online: August 16, 2004
Accepted:
July 24,
1998
Received in revised form:
July 24,
1998
Received:
March 31,
1998
Identification
Copyright
© 1999 Excerpta Medica Inc. Published by Elsevier Inc. All rights reserved.
