Volume 44, Issue 11 pp. 1555-1561

Molecular and serologic tracing of a transfusion-transmitted hepatitis A virus

Peter Gowland

Corresponding Author

Peter Gowland

From the Blood Transfusion Service Berne, Swiss Red Cross; and the Department of Hematology and Central Hematology Laboratory, Division of Transfusion Medicine, Inselspital, University of Berne, Berne, Switzerland.

Peter Gowland, Blood Transfusion Service Berne, Swiss Red Cross, Berne, Switzerland, Murtenstrasse 133, CH 3008 Berne, Switzerland; e-mail: [email protected].Search for more papers by this author
Stefano Fontana

Stefano Fontana

From the Blood Transfusion Service Berne, Swiss Red Cross; and the Department of Hematology and Central Hematology Laboratory, Division of Transfusion Medicine, Inselspital, University of Berne, Berne, Switzerland.

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Christoph Niederhauser

Christoph Niederhauser

From the Blood Transfusion Service Berne, Swiss Red Cross; and the Department of Hematology and Central Hematology Laboratory, Division of Transfusion Medicine, Inselspital, University of Berne, Berne, Switzerland.

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Behrouz Mansouri Taleghani

Behrouz Mansouri Taleghani

From the Blood Transfusion Service Berne, Swiss Red Cross; and the Department of Hematology and Central Hematology Laboratory, Division of Transfusion Medicine, Inselspital, University of Berne, Berne, Switzerland.

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First published: 22 October 2004
Citations: 45

This work was partially supported by an unrestricted grant of Gambro BCT SA, Zaventum, Belgium.

Abstract

BACKGROUND: The transmission of hepatitis A virus (HAV) via blood transfusion has not been evidenced by molecular tracing so far.

CASE REPORT: A 33-year-old asymptomatic female volunteer made a whole-blood donation. Thirteen days later an acute HAV infection was diagnosed. Retrospectively, a high viral load was measured by quantitative reverse transcription polymerase chain reaction (RT-PCR) in the quarantine fresh-frozen plasma (1.4 × 106 geq/mL), whereas immunoglobulin M (IgM) and G (IgG)/IgM anti-HAV were not detectable and the alanine aminotransferase levels not elevated. The red blood cells have just been transfused on Day 14. The 63-year-old male recipient already was HAV seropositive. He did not develop clinical symptoms of HAV and anti-HAV IgM was not detected. Seventy-five days later, a 25-fold increase in the anti-HAV IgG/IgM titer was observed. Demonstrable HAV ribonucleic acid (RNA) in the recipient by means of RT-PCR on Day 6, but not on Days 1 and 75, suggests that a transient reinfection did occur. Analyzed sequences of the HAV RNA in the donor and recipient were identical.

CONCLUSION: For the first time, transfusion-transmitted HAV was evidenced by molecular and serologic tracing. The transmitted HAV can survive and replicate for a limited period despite the presence of anti-HAV IgG.

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