Exposure to holoendemic malaria results in elevated Epstein-Barr virus loads in children

被引:146
作者
Moormann, AM
Chelimo, K
Sumba, OP
Lutzke, ML
Ploutz-Snyder, R
Newton, D
Kazura, J
Rochford, R
机构
[1] SUNY Upstate Med Univ, Dept Microbiol & Immunol, Syracuse, NY 13210 USA
[2] Ctr Vector Biol & Control Res, Kenya Med Res Inst, Kisumu, Kenya
[3] SUNY Upstate Med Univ, Ctr Outcomes Res & Evaluat, Syracuse, NY 13210 USA
[4] Univ Michigan, Dept Epidemiol, Ann Arbor, MI 48109 USA
[5] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA
[6] Case Western Reserve Univ, Ctr Global Hlth & Dis, Cleveland, OH 44106 USA
关键词
D O I
10.1086/428910
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:1233 / 1238
页数:6
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