A prospective study on tt virus infection in transfusion-dependent patients with β-thalassemia

Daniele Prati, Yu Huei Lin, Claudia De Mattei, Jen Kuei Liu, Elena Farma, Latha Ramaswamy, Alberto Zanella, Helen Lee, Paolo Rebulla, Jean Pierre Allain, Girolamo Sirchia, Benjamin Chen

Research output: Contribution to journalArticlepeer-review

Abstract

A novel DNA virus designated TT virus (TTV) has been reported to be involved in the development of posttransfusion non-A-C hepatitis. We evaluated the frequency and natural course of TTV infection in a cohort of transfusion-dependent thalassemic patients in a 3-year follow-up study. Ninety-three serum hepatitis C virus (HCV) antibody-negative patients (median age of 8 years; range, 0 to 25) from eight centers were studied. Of them, 34 (37%) had an abnormal alanine-aminotransferase (ALT) baseline pattern, and the other 12 (13%) showed ALT flare-ups during the follow-up. TTV DNA in patient sera collected at the time of enrollment and at the end of follow-up was determined by polymerase chain reaction (PCR). In parallel, serum samples from 100 healthy blood donors were also tested. At baseline, 87 patient sera (93.5%) tested positive for the TTV DNA. Of these TTV DNA-positive patients, 84 (96.5%) remained viremic at the end of the study period. Of the 6 TTV DNA- negative patients, 3 acquired TTV infection during follow-up. However, no definite relation was observed between the results of TTV DNA determination and ALT patterns. TTV viremia was also detectable in 22% of blood donors. In conclusion, TTV infection is frequent and persistent among Italian transfusion-dependent patients. The high rate of viremia observed in healthy donors indicates that the parenteral route is not the only mode of TTV spread.

Original languageEnglish
Pages (from-to)1502-1505
Number of pages4
JournalBlood
Volume93
Issue number5
Publication statusPublished - Mar 1 1999

ASJC Scopus subject areas

  • Hematology

Fingerprint Dive into the research topics of 'A prospective study on tt virus infection in transfusion-dependent patients with β-thalassemia'. Together they form a unique fingerprint.

Cite this