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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
biochemistry, genetics and molecular biology
A molecular link between malaria and Epstein-Barr virus reactivation
PLoS Pathogens, Volume 3, No. 6, Year 2007
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Description
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-gammaglobulinemia. We recently identified the cystein-rich inter-domain region 1α (CIDR1α) 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 mechanisms of interaction between CIDR1α and EBV in the context of B cells. We show that CIDR1α binds to the EBV-positive B cell line Akata and increases the number of cells switching to the viral lytic cycle as measured by green fluorescent protein (GFP) expression driven by a lytic promoter. The virus production in CIDR1α-exposed cultures was directly proportional to the number of GFP-positive Akata cells (lytic EBV) and to the increased expression of the EBV lytic promoter BZLF1. Furthermore, CIDR1α stimulated the production of EBV in peripheral blood mononuclear cells derived from healthy donors and children with BL. Our results suggest that P. falciparum antigens such as CIDR1α can directly induce EBV reactivation during malaria infection that may increase the risk of BL development for children living in malaria-endemic areas. To our knowledge, this is the first report to show that a microbial protein can drive a latently infected B cell into EBV replication. © 2007 Chêne et al.
Authors & Co-Authors
Chêne, Arnaud
Sweden, Stockholm
Karolinska Institutet
Sweden, Solna
Public Health Agency of Sweden
Donati, Daria
Sweden, Stockholm
Karolinska Institutet
Guerreiro-Cacais, André Ortlieb
Sweden, Stockholm
Karolinska Institutet
United States, Baltimore
Johns Hopkins University
Levitsky, Victor
Sweden, Stockholm
Karolinska Institutet
United States, Baltimore
Johns Hopkins University
Chen, Qijun
Sweden, Solna
Public Health Agency of Sweden
Falk, Kerstin Ingrid
Sweden, Stockholm
Karolinska Institutet
Sweden, Solna
Public Health Agency of Sweden
Orem, Jackson
Uganda, Kampala
Uganda Cancer Institute
Kironde, Fred Alexander Sekaza
Uganda, Kampala
Makerere University
Wahlgren, Mats
Sweden, Stockholm
Karolinska Institutet
Sweden, Solna
Public Health Agency of Sweden
Bejarano, Maria Teresa
Sweden, Stockholm
Karolinska Institutet
Statistics
Citations: 179
Authors: 10
Affiliations: 5
Identifiers
Doi:
10.1371/journal.ppat.0030080
ISSN:
15537366
e-ISSN:
15537374
Research Areas
Cancer
Infectious Diseases
Maternal And Child Health