Abstract
BackgroundInfectious 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.MethodsHHV-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).ResultsHHV-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.ConclusionThis study confirms the absence of role of HHV-6 in the genesis of acute leukemia but the virus was reactivated after chemotherapy treatment.
Highlights
Infectious etiology in lymphoproliferative diseases has always been suspected
human herpesvirus-6 (HHV-6) detection was significantly higher at remission than at diagnosis (p = 0.04) or during aplasia (p = 0.005), and higher at relapse than at diagnosis (p = 0.06) or during aplasia (p = 0.02)
As observed for the blood samples, HHV-6 detection rate increased in samples at remission (p = 0.01) and at relapse (p = 0.03) compared to diagnosis
Summary
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. Human herpesvirus-6 (HHV-6) belongs to the Roseolovirus genus of the Betaherpesvirinae subfamily of the Herpesviridae family. HHV-6 genome is a linear, double-stranded DNA molecule, 160 to 162 kpb in size, flanked by terminal direct repeats (DRL and DRR) of 8 to 9 kpb. The genes in UL are termed U1 to U100 and open reading frames (ORFs) within the direct repeats are designated as DR1 to DR7 [3]
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