Open Access Research article

Quantitative analysis of human herpesvirus-6 genome in blood and bone marrow samples from Tunisian patients with acute leukemia: a follow-up study

Nefzi Faten1*, Gautheret-Dejean Agnès23, Ben Fredj Nadia1, Abid Ben Salem Nabil1, Zaier Monia4, Khelif Abderrahim4, Agut Henri23, Feki Salma5 and Aouni Mahjoub1

Author Affiliations

1 Laboratory of Transmissible Diseases and Biological Active Substances, LR99-ES27, Faculty of Pharmacy, University of Monastir, Monastir, Tunisia

2 UPMC Univ Paris 06, ER1 DETIV, Paris, France

3 Laboratory of Virology, Pitié-Salpêtrière Hospital AP-HP, Paris, France

4 Department of Clinical Hematology, Farhat Hached Hospital, Sousse, Tunisia

5 Department of Clinical Biology, Faculty of Pharmacy, Monastir, Tunisia

For all author emails, please log on.

Infectious Agents and Cancer 2012, 7:31  doi:10.1186/1750-9378-7-31

Published: 12 November 2012

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.

Conclusion

This study confirms the absence of role of HHV-6 in the genesis of acute leukemia but the virus was reactivated after chemotherapy treatment.

Keywords:
Human herpesvirus-6; Acute leukemia; Viral load; Bone marrow; Whole blood; Chemotherapy