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

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    Authors
    Moormann, Ann M.
    Chelimo, Kiprotich
    Sumba, Peter Odada
    Tisch, Daniel J.
    Rochford, Rosemary A.
    Kazura, James W.
    UMass Chan Affiliations
    Department of Pediatrics
    Department of Quantitative Health Sciences
    Document Type
    Journal Article
    Publication Date
    2007-02-15
    Keywords
    Adolescent
    Animals
    Burkitt Lymphoma
    Child
    Child, Preschool
    Herpesvirus 4, Human
    Humans
    Kenya
    Malaria, Falciparum
    Plasmodium falciparum
    T-Lymphocytes
    Biostatistics
    Epidemiology
    Health Services Research
    Immunology and Infectious Disease
    Pediatrics
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    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.
    Source
    J Infect Dis. 2007 Mar 15;195(6):799-808. Epub 2007 Feb 6. Link to article on publisher's site
    DOI
    10.1086/511984
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/47254
    PubMed ID
    17299709
    Related Resources
    Link to Article in PubMed
    Rights
    © 2007 by the Infectious Diseases Society of America.
    ae974a485f413a2113503eed53cd6c53
    10.1086/511984
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    Population and Quantitative Health Sciences Publications

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