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J Infect Dis. 2007 Mar 15;195(6):799-808. Epub 2007 Feb 6.

Exposure to holoendemic malaria results in suppression of Epstein-Barr virus-specific T cell immunosurveillance in Kenyan children.

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  • 1Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH, 44106, USA. moorms@case.edu

Abstract

BACKGROUND:

Malaria and Epstein-Barr virus (EBV) infection are cofactors in the pathogenesis of endemic Burkitt lymphoma (eBL). The mechanisms by which these pathogens predispose to eBL are not known.

METHODS:

Healthy Kenyan children with divergent malaria exposure were measured for responses to EBV latent and lytic antigens by interferon (IFN)- gamma enzyme-linked immunospot (ELISPOT) assay and interleukin (IL)-10 ELISA. Phytohemagglutinin (PHA), purified protein derivative (PPD), and T cell epitope peptides derived from merozoite surface protein (MSP)-1, a malaria blood-stage antigen, were also evaluated.

RESULTS:

Children 5-9 years old living in an area holoendemic for malaria had significantly fewer EBV-specific IFN- gamma responses than did children of the same age living in an area with unstable malaria transmission. This effect was not observed for children <5 years old or those >9 years old. In contrast, IFN- gamma responses to PHA, PPD, and Plasmodium falciparum MSP-1 peptides did not significantly differ by age. IL-10 responses to EBV lytic antigens, PPD, and PHA correlated inversely with malaria exposure regardless of age.

CONCLUSIONS:

Children living in malaria-holoendemic areas have diminished EBV-specific T cell immunosurveillance between the ages of 5 and 9 years, which coincides with the peak age incidence of eBL.

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