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Human herpesvirus-6 infection: A prospective study evaluating HHV-6 DNA levels in liver from children with acute liver failure

✍ Scribed by Laurent Chevret; David Boutolleau; Nadia Halimi-Idri; Sophie Branchereau; Catherine Baujard; Monique Fabre; Agnès Gautheret-Dejean; Dominique Debray


Publisher
John Wiley and Sons
Year
2008
Tongue
English
Weight
101 KB
Volume
80
Category
Article
ISSN
0146-6615

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✦ Synopsis


Abstract

The aim of this prospective study was to investigate the role of HHV‐6 infection in children with acute onset of liver failure using real‐time quantitative PCR. Twenty‐three children (median age, 24 months) were included: 6 cases of fulminant hepatic failure of undetermined cause (group 1); 4 cases of fulminant hepatic failure of recognized cause (group 2); 3 cases of acute decompensation of chronic liver disease (group 3); and 10 cases of chronic liver disease (group 4). HHV‐6 genomic DNA was detected and quantified using real‐time PCR in plasma and livers obtained at the time of transplantation. HHV6‐DNA detection rate was significantly higher among groups 1, 2, and 3 compared to group 4 (76.9% vs. 20% P = 0.02). Viral loads ranged from 6 to 32,500 copies/106 cells. Significantly higher viral loads were found in 4 of 9 children with acute onset of liver failure of unknown origin (group 1, n = 3; group 3, n = 1) and 1 child with fulminant autoimmune hepatitis (group 2) (P = 0.03). These results strongly support the hypothesis that HHV‐6 may cause fulminant hepatic failure and acute decompensation of chronic liver disease in children. Nevertheless, a threshold viral load value still remains to be determined. J. Med. Virol. 80:1051–1057, 2008. © 2008 Wiley‐Liss, Inc.