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Exposure to Holoendemic Malaria Results in Elevated Epstein‐Barr Virus Loads in Children
Author(s) -
Ann M. Moormann,
Kiprotich Chelimo,
O.P. Sumba,
Mary L. Lutzke,
Robert PloutzSnyder,
Duane W. Newton,
James W. Kazura,
Rosemary Rochford
Publication year - 2005
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/428910
Subject(s) - malaria , transmission (telecommunications) , medicine , epstein–barr virus , virology , viral load , immunology , kenya , virus , polymerase chain reaction , biology , genetics , ecology , electrical engineering , engineering , gene
Perennial and intense malaria transmission (holoendemic malaria) and Epstein-Barr virus (EBV) infection are 2 cofactors in the pathogenesis of endemic Burkitt lymphoma (eBL). In the present study, we compared EBV loads in children living in 2 regions of Kenya with differing malaria transmission intensities: Kisumu District, where malaria transmission is holoendemic, and Nandi District, where malaria transmission is sporadic. For comparison, blood samples were also obtained from US adults, Kenyan adults, and patients with eBL. Extraction of DNA from blood and quantification by polymerase chain reaction give an EBV load estimate that reflects the number of EBV-infected B cells. We observed a significant linear trend in mean EBV load, with the lowest EBV load detected in US adults and increasing EBV loads detected in Kenyan adults, Nandi children, Kisumu children, and patients with eBL, respectively. In addition, EBV loads were significantly higher in Kisumu children 1-4 years of age than in Nandi children of the same age. Our results support the hypothesis that repeated malaria infections in very young children modulate the persistence of EBV and increase the risk for the development of eBL.

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