title: Quantitative analysis of human herpesvirus-6 genome in blood and bone marrow samples from Tunisian patients with acute leukemia: a follow-up study.
abstract: BACKGROUND
  Infectious etiology in lymphoproliferative diseases has always been suspected. The pathogenic roles of human herpesvirus-6 (HHV-6) in acute leukemia have been of great interest. Discordant results to establish a link between HHV-6 activation and the genesis of acute leukemia have been observed. The objective of this study was to evaluate a possible association between HHV-6 infection and acute leukemia in children and adults, with a longitudinal follow-up at diagnosis, aplasia, remission and relapse.
  
  
  METHODS
  HHV-6 load was quantified by a quantitative real-time PCR in the blood and bone marrow samples from 37 children and 36 adults with acute leukemia: 33 B acute lymphoblastic leukemia (B-ALL), 6 T acute lymphoblastic leukemia (T-ALL), 34 acute myeloid leukemia (AML).
  
  
  RESULTS
  HHV-6 was detected in 15%, 8%, 30% and 28% of the blood samples at diagnosis, aplasia, remission and relapse, respectively. The median viral loads were 138, 244, 112 and 78 copies/million cells at diagnosis, aplasia, remission and relapse, respectively. In the bone marrow samples, HHV-6 was detected in 5%, 20% and 23% of the samples at diagnosis, remission and relapse, respectively. The median viral loads were 34, 109 and 32 copies/million cells at diagnosis, remission and relapse, respectively. According to the type of leukemia at diagnosis, HHV-6 was detected in 19% of the blood samples and in 7% of the bone marrow samples (with median viral loads at 206 and 79 copies/million cells, respectively) from patients with B-ALL. For patients with AML, HHV-6 was present in 8% of the blood samples and in 4% of the bone marrow samples (with median viral loads at 68 and 12 copies/million cells, respectively). HHV-6 was more prevalent in the blood samples from children than from adults (25% and 9%, respectively) and for the bone marrow (11% and 0%, respectively). All typable HHV-6 were HHV-6B species. No link was shown between neither the clinical symptoms nor the abnormal karyotype and HHV-6 activation. A case of HHV-6 chromosomal integration was shown in one patient with AML.
  
  
  CONCLUSIONS
  This study confirms the absence of role of HHV-6 in the genesis of acute leukemia but the virus was reactivated after chemotherapy treatment.
authors.affiliation: Laboratory of Transmissible Diseases and Biological Active Substances, LR99-ES27, Faculty of Pharmacy, University of Monastir, Monastir, Tunisia. fatennef@yahoo.fr.
authors.forename: Nefzi
authors.initials: N
authors.lastname: Faten
authors.forename: Gautheret-Dejean
authors.initials: GD
authors.lastname: Agnès
authors.forename: Ben Fredj
authors.initials: BF
authors.lastname: Nadia
authors.forename: Abid Ben Salem
authors.initials: AB
authors.lastname: Nabil
authors.forename: Zaier
authors.initials: Z
authors.lastname: Monia
authors.forename: Khelif
authors.initials: K
authors.lastname: Abderrahim
authors.forename: Agut
authors.initials: A
authors.lastname: Henri
authors.forename: Feki
authors.initials: F
authors.lastname: Salma
authors.forename: Aouni
authors.initials: A
authors.lastname: Mahjoub