Symptomatic parvovirus B19 infection caused by blood component transfusion

• Published in: Transfusion (Philadelphia, Pa.) Pa.), 2011-09, Vol.51 (9), p.1887-1895
• Main Authors: Satake, Masahiro, Hoshi, Yuji, Taira, Rikizo, Momose, Shun-ya, Hino, Satoru, Tadokoro, Kenji
• Format: Article
• Language: English
• Subjects: Adult; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Blood Component Transfusion - adverse effects; Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis; Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care; Female; Humans; Intensive care medicine; Male; Medical sciences; Middle Aged; Parvoviridae Infections - blood; Parvoviridae Infections - etiology; Parvoviridae Infections - virology; Parvovirus B19, Human - pathogenicity; Polymerase Chain Reaction; Transfusions. Complications. Transfusion reactions. Cell and gene therapy
• ISSN: 0041-1132; 1537-2995
• DOI: 10.1111/j.1537-2995.2010.03047.x

BACKGROUND: Although a risk of transfusion‐transmitted human parvovirus B19V (TT‐B19V) infection has been a concern, there have been very few reports of clinically relevant TT‐B19V caused by the transfusion of a B19V‐containing blood component. It has therefore been a matter of debate whether a universal B19V screening with an appropriate sensitivity is required. STUDY DESIGN AND METHODS: Through the Japanese Red Cross hemovigilance system, clinical reports on possible TT‐B19V were collected from 1999 to 2008, during which B19V donor screening (sensitivity, 1010 IU/mL) was conducted and repository blood samples from donors were available. RESULTS: Eight patients with TT‐B19V caused by component transfusion have been identified. Four patients developed sustained anemia and pure red blood cell (RBC) aplasia and one patient developed pancytopenia. The underlying diseases in these five patients were either hematologic malignancy or hemolytic diseases. The viral loads of the responsible components for these cases ranged from 103 to 108 IU/mL. Two patients who underwent surgical treatment without any hematologic disorder exhibited only moderate symptoms. The B19V DNA sequence identity between a patient and the linked blood donor was confirmed in five of the eight patients. All of the components responsible for the eight cases were positive for anti‐B19V immunoglobulin (Ig)M. CONCLUSION: Vulnerability to serious B19V‐related hematologic disorders depended on the patient's underlying disease state of an enhanced erythropoiesis, not on the viral load of the component transfused. To prevent clinically relevant TT‐B19V, a strategy is suggested in which patients at risk of acquiring RBC aplasia or pancytopenia are targeted.