Individuals who are chronically infected with certain pathogens are at increased risk of developing lymphomas, cancers of the antibody-producing B lymphocytes. For example, Burkitt's lymphoma, a common form of childhood cancer, is ten times more frequent in areas of equatorial Africa that are endemic for malaria. How the malaria-causing parasite promotes blood cell cancer was not known.

Researchers discovered that during prolonged immune responses to malaria, B lymphocytes multiply extensively and show prolonged expression of an enzyme called AID (activation-induced cytidine deaminase).

Normally, AID mutates DNA at antibody genes to promote shuffling of DNA, which generates the diversity of antibodies so crucial for combating infections. However, the team found that in malaria-infected B lymphocytes, AID instead wreaks widespread havoc, causing DNA rearrangements at other genes, including those involved in the development of cancer.