HHV-6 not an etiologic player in pediatric acute lymphoblastic leukemia

NEW YORK (Reuters Health) - Results of a French study do not support a role for human herpesvirus-6 (HHV-6) infection in the development of childhood acute lymphoblastic leukemia.

In a report in the April issue of the Journal of Medical Virology, researchers note that an infectious etiology in pediatric acute lymphoblastic leukemia has been suspected and the role of HHV-6 has been suggested. However, several studies that have tried to establish a link between HHV-6 and...

NEW YORK (Reuters Health) - Results of a French study do not support a role for human herpesvirus-6 (HHV-6) infection in the development of childhood acute lymphoblastic leukemia.

In a report in the April issue of the Journal of Medical Virology, researchers note that an infectious etiology in pediatric acute lymphoblastic leukemia has been suspected and the role of HHV-6 has been suggested. However, several studies that have tried to establish a link between HHV-6 and hematological malignancies have yielded discordant results.

Dr. Elisa Seror, of Hopital Trousseau in Paris, and colleagues used quantitative real-time polymerase chain reaction to measure HHV-6 genome copy number in bone marrow and peripheral blood samples obtained from 36 children with acute lymphoblastic leukemia.

Seventy-seven samples were tested: 36 samples at the time of diagnosis and 41 at complete remission. According to the researchers, 13.6% of the diagnosis samples and 34.1% of the complete remission samples were positive for HHV-6 genome.

"Viral load was low with values lower at diagnosis (median copy number = 22.9 per million cells) than at complete remission (median copy number = 60.1 per million cells)," Dr. Seror and colleagues report.

"These results argue against an etiological relationship between HHV-6 infection and the genesis of acute lymphoblastic leukemia in childhood," they conclude.

The results, they add, "support the hypothesis of viral latency in bone marrow, probably associated with the progenitors, but argue against the possibility of infection of leukemic cells, raising again the question of the mechanism of virus entry. They also support the possibility of virus reactivation in immunocompromised hosts."

J Med Virol 2008;80:689-693.