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Archives of Disease in Childhood 1999;80:429-432; doi:10.1136/adc.80.5.429
Copyright © 1999 BMJ Publishing Group Ltd & Royal College of Paediatrics and Child Health.
Arch Dis Child 1999;80:429-432 ( May )

GB virus C/hepatitis G virus infection in HIV infected patients with haemophilia despite treatment with virus inactivated clotting factor concentrates

Joachim Woelfle,a Thomas Berg,c Ralf Bialek,a Klaus Michael Keller,a Wolfgang Effenberger,b Norbert Wagnera

a Department of Paediatrics, Children's Hospital, University of Bonn, 53113 Bonn, Germany, b Institute of Experimental Haematology and Transfusion Medicine, University of Bonn, Campus Charité, c Virchow Hospital, Department of Hepatology/ Gastroenterology, University of Berlin, 13353 Berlin, Germany

Correspondence to: Dr Woelfle, Zentrum f. Kinderheilkunde, Rhein. Friedrich-Wilhelms-Universität, Adenauerallee 119, D-53113 Bonn, Germany.

Accepted 23 December 1998

AIM---To determine the frequency of GB virus C (GBV-C)/hepatitis G virus (HGV) infection before and after switch to the use of virus inactivated concentrates in haemophiliac patients infected with human immunodeficiency virus (HIV).
PATIENTS AND METHODS---Initial and follow up sera from 49 children with haemophilia were analysed for the presence of GBV-C/HGV RNA and antibodies to HGV (anti-HGV). All patients had been infected with HIV while receiving concentrates without virus inactivation before 1984 and were subsequently treated with virus inactivated concentrates.
RESULTS---In the first available serum sample (1987 or later), two of 49 patients were GBV-C/HGV RNA positive and two further patients were anti-HGV positive. During follow up (mean, 6 years), 14 patients developed markers of GBV-C/HGV infection. Eleven of these had received no blood products except clotting factor concentrates that had been prepared with virus inactivation.
CONCLUSIONS---Despite being treated with virus inactivated clotting factor concentrates, HIV positive patients with haemophilia are at an increased risk of manifesting GBV-C/HGV infection. We hypothesise that GBV-C/HGV is transmitted by these clotting factor concentrates. However, we cannot rule out the emergence of markers of GBV-C/HGV infection as a result of the progression of immune impairment in the course of HIV infection.


Keywords: hepatitis G virus; GB virus C; haemophilia; HIV


© 1999 by Archives of Disease in Childhood

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