June 9, 2007 Endemic Burkitt lymphoma is a form of cancer that accounts for up to 74% of malignant disorders in children in equatorial Africa. Malaria and Epstein-Barr virus (EBV) are known cofactors in its development, but to date, their relative contribution has not been well understood. In a new study published online in the open-access journal PLoS Pathogens, researchers at the Karolinska Institutet in Stockholm explain how certain Plasmodium falciparum antigens directly induce Epstein-Barr virus (EBV) reactivation, increasing the risk of Burkitt lymphoma.
EBV is a ubiquitous virus that establishes a lifelong persistence following primary infection. How EBV affects its host hinges on a balance between viral latency, viral replication, and host immune responses. Generally harmless in almost every host and rarely a cause of disease, reactivation of EBV has been causally associated with various cancers. Acute malaria infection is known to increase the level of circulating EBV, but the precise mechanisms through which this virus reactivation occurs had been previously unknown.
Now, Arnaud Chene and colleagues have identified CIDRla as the first microbial protein able to spur a latently EBV-infected cell into active production. Their results suggest that P. falciparum-derived proteins can lead to a direct reactivation of EBV during acute malaria infection, increasing the risk of Burkitt lymphoma development for children living in malaria-endemic areas.
This work was supported by grants from the Karolinska Institutet, the Swedish International Development Cooperation, Malaria and EBV Reactivation Agency (Sida/SAREC), Barncancerfonden, the Swedish Research Council (VR), and the Swedish Foundation for Strategic Research.
Article: Chene A, Donati D, Guerreiro-Cacais AO, Levitsky V, Chen Q, et al. (2007) A molecular link between malaria and Epstein-Barr virus reactivation. PLoS Pathog 3(6): e80. doi:10.1371/journal.ppat.0030080
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