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TT virus in frequently transfused patients

      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 (
      • Linnen J
      • Wages J
      • Zhang-Keck Z.Y
      • et al.
      Molecular cloning and disease association of hepatitis G virus a transfusion-transmissible agent.
      ). Subsequently, however, it was shown that this virus rarely causes hepatitis, even in immunosuppressed patients (
      • Miyakawa Y
      • Mayumi M
      Hepatitis G virus—a true hepatitis or an accidental tourist?.
      ,
      • Kanda Y
      • Chiba S
      • Kami M
      • et al.
      Quantitation of hepatitis G virus RNA in bone marrow transplant recipients.
      ). Recently, a novel DNA virus, named TT virus, was cloned from serum of a patient with posttransfusion hepatitis (
      • Nishizawa T
      • Okamoto H
      • Konishi K
      • et al.
      A novel DNA virus (TTV) associated with elevated transaminase levels in posttransfusion hepatitis of unknown etiology.
      ). 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 (
      • Nishizawa T
      • Okamoto H
      • Konishi K
      • et al.
      A novel DNA virus (TTV) associated with elevated transaminase levels in posttransfusion hepatitis of unknown etiology.
      ). 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.
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      References

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        • et al.
        Molecular cloning and disease association of hepatitis G virus.
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