Background. Indirect epidemiologic evidences have suggested that viral infections may represent an important risk factor in the etiological mechanisms of B cell precursor lymphoblastic leukemia (BpALL), specially common-ALL. Parvovirus B19 (PvB19) is associated with aplastic crisis, thrombocytopenia, and congenital anemia. Five studies have reported the concurrent PvB19 infection in pediatric ALL. In a view of the increasing contest about the direct or indirect role of viral infection in ALL, we evaluated the possible associations of PvB19 and herpes virus 6 (HHV-6) in samples from children suffering from hematological disorders in order to estimate the magnitude of risk of association with common-BpALL.

Material and Methods. A total of 659 blood samples were randomly selected to perform the serological tests. They were part of diagnostic samples referred to CPq-INCA-Rio de Janeiro, Brazil, from 2002–2006, for diagnostic purpose. Blood samples were exclusively selected from patients in whom samples were taken at the time of the onset of sickness. The diagnosis of BpALL was based on immunophenotyping methods according to EGIL criteria. The presence of serum antibodies for PvB19 and HHV-6 were determinate by enzyme-linked immunosorbent assay. Statistical analyses were conducted using SPSS for Windows 11.0. All p values were two sided; p<0.05 was considered statistically significant.

Results. Common-ALL (n=176) and non-leukemic samples (n=107) considered as control group were stratified according to age-groups at diagnosis. Age distribution was:

  1. less than 2 years (15.5%);

  2. 2–6 years-old (46.0%), and

  3. 7–12 years-old (17.7%).

The estimation of associated risk PvB19 IgG+ antibodies with common-BpALL was OR 0.53 95% CI (0.52–0.54); whereas HHV-6 IgG was OR 2.36, 95% CI (1.08–5.17).

Conclusions. We find out a higher prevalence of HHV-6 antibodies in patients with common-BpALL, suggesting an association between HHV-6 infection e common-BpALL in Brazilian children. There is a long history in developed countries regarding the role of infections in leukemogenesis process. Further tests are necessary to confirm these results.

Disclosures: No relevant conflicts of interest to declare.

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