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An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells
Published on: August 15, 2012
A molecular link between malaria and Epstein-Barr virus reactivation
Arnaud Chêne1, Daria Donati, André Ortlieb Guerreiro-Cacais
1Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Plos Pathogens
|June 15, 2007
Summary
Malaria protein CIDR1alpha reactivates Epstein-Barr virus (EBV) in B cells, potentially increasing Burkitt lymphoma risk in children in malaria-endemic regions.
Area of Science:
- Immunology
- Virology
- Oncology
Background:
- Endemic Burkitt lymphoma (BL) is a pediatric cancer linked to malaria and Epstein-Barr virus (EBV).
- The specific roles of malaria and EBV in BL development are not fully understood.
- EBV establishes lifelong latency in B cells, while malaria impacts B cell populations.
Purpose of the Study:
- To investigate the interaction between a malaria antigen, CIDR1alpha, and EBV in B cells.
- To determine if CIDR1alpha can induce EBV reactivation.
Main Methods:
- Exposure of EBV-positive B cell lines (Akata) and primary cells to CIDR1alpha.
- Measurement of EBV lytic cycle activation using GFP expression and viral production.
- Analysis of EBV promoter activity (BZLF1).
Main Results:
- CIDR1alpha binds to EBV-positive B cells and increases EBV lytic cycle reactivation.
- Increased virus production correlated with CIDR1alpha exposure and EBV lytic activity.
- CIDR1alpha stimulated EBV production in peripheral blood mononuclear cells from healthy donors and BL patients.
Conclusions:
- Plasmodium falciparum antigens like CIDR1alpha can directly trigger EBV reactivation in latently infected B cells.
- This reactivation may elevate the risk of endemic Burkitt lymphoma in children in malaria-prone areas.
- This study is the first to demonstrate a microbial protein driving EBV replication from latency.
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