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.
No takes yet. Share an insight, caveat, or question.
Chevret et al. (2008) studied this question.
Synapse has enriched 5 related papers. Consider them for comparative context: