a molecular link between malaria and epstein–barr virus reactivation疟疾和巴尔病毒再活化分子之间的联系.pdfVIP

A Molecular Link between Malaria and Epstein–Barr Virus Reactivation ˆ 1,2,3[ 1[* ´ 2¤ 2¤ 3 Arnaud Chene , Daria Donati , Andre Ortlieb Guerreiro-Cacais , Victor Levitsky , Qijun Chen , Kerstin I. Falk2,3 4 5 2,3 1,2 , Jackson Orem , Fred Kironde , Mats Wahlgren , Maria Teresa Bejarano 1 Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden, 2 Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden, 3 Swedish Institute for Infectious Disease Control, Stockholm, Sweden, 4 Uganda Cancer Institute, Kampala, Uganda, 5 Department of Biochemistry, Faculty of Medicine, Makerere University, Kampala, Uganda Although malaria and Epstein–Barr (EBV) infection are recognized cofactors in the genesis of endemic Burkitt lymphoma (BL), their relative contribution is not understood. BL, the most common paediatric cancer in equatorial Africa, is a high-grade B cell lymphoma characterized by c-myc translocation. EBV is a ubiquitous B lymphotropic virus that persists in a latent state after primary infection, and in Africa, most children have sero-converted by 3 y of age. Malaria infection profoundly affects the B cell compartment, inducing polyclonal activation and hyper-gammaglobu- linemia. We recently identified the cystein-rich inter-domain region 1a (CIDR1a) of the Plasmodium falciparum membrane protein 1 as a polyclonal B cell activator that preferentially activates the memory compartment, where EBV is known to persist. Here, we have addressed the mechanism