摘要

The development of endemic Burkitt's lymphoma (eBL) is closely associated with Epstein-Barr virus (EBV) infection and holoendemic malaria infections. The role of EBV in the development of malignancy has been studied in depth, but there is still little known about the mechanisms by which malaria affects Burkitt's lymphomagenesis. Activation induced cytidine deaminase (AID) expression is necessary for the introduction of c-myc translocations that are characteristic of BL, but a link between AID and EBV or malaria is unclear. To determine whether frequency of malaria exposure leads to increased AID expression in peripheral blood mononuclear cells (PBMC) we examined two cohorts of children in western Kenya with endemic and sporadic malaria transmission dynamics. High frequency of malaria exposure led to increased expression of AID, which coincided with decreases in the IgM(+) memory B cells. In the children from the malaria endemic region, the presence of a detectible EBV viral load was associated with higher AID expression compared to children with undetectable EBV, but this effect was not seen in children with sporadic exposure to malaria. This study demonstrates that intensity of malaria transmission correlates with AID expression levels in the presence of EBV suggesting that malaria and EBV infection have a synergistic effect on the development of c-myc translocations and BL. What's New? Activation-induced cytidine deaminase (AID) expression has been linked to translocations in the c-myc transcription factor that can cause Burkitt's lymphoma, a tumor closely associated with Epstein Barr Virus (EBV) and malaria infections. Here the authors demonstrate a first link between AID expression and exposure to malaria in the peripheral blood of children. They further show that AID expression is linked to detectable EBV in children living in a region of high malaria transmission. These findings shed new light on how malaria and EBV co-infections can increase the risk of developing Burkitt's lymphoma.

  • 出版日期2015-3-15