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    Malaria - how this parasitic infection aids and abets EBV-associated Burkitt lymphomagenesis

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    Authors
    Moormann, Ann M.
    Bailey, Jeffrey A.
    UMass Chan Affiliations
    Program for Bioinformatics and Integrative Biology
    Program in Molecular Medicine
    Document Type
    Journal Article
    Publication Date
    2016-10-01
    Keywords
    UMCCTS funding
    Hemic and Lymphatic Diseases
    Immunology and Infectious Disease
    Neoplasms
    Parasitic Diseases
    Translational Medical Research
    Virology
    Virus Diseases
    
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5102755/
    Abstract
    Burkitt lymphoma (BL) is >90% EBV-associated when this pediatric cancer is diagnosed in regions heavily burden by endemic Plasmodium falciparum malaria and thus has been geographically classified as endemic BL. The incidence of endemic BL is 10-fold higher compared to BL diagnosed in non-malarious regions of the world. The other forms of BL have been classified as sporadic BL which contain EBV in approximately 30% of cases and immunodeficiency BL which occurs in HIV-infected adults with approximately 40% of tumors containing EBV. Within malaria endemic regions, epidemiologic studies replicating Denis Burkitt's seminal observation continue to show differences in endemic BL incidence linked to intensity of malaria transmission. However, the mechanisms by which malaria contributes to B cell tumorigenesis have not been resolved to the point of designing cancer prevention strategies. The focus of this review is to summarize our current knowledge regarding the influence of prolonged, chronic malaria exposure on defects in immunosurveillance that would otherwise control persistent EBV infections. And thus, set the stage for ensuing mechanisms by which malaria could instigate B cell activation and aberrant activation-induced cytidine deaminase expression initiating somatic hypermutation and thereby increasing the likelihood of an Ig/Myc translocation, the hallmark of all BL tumors. Malaria appears to play multiple, sequential and simultaneous roles in endemic BL etiology; the complexity of these interactions are being revealed by applying computational methods to human immunology. Remaining questions yet to be addressed and prevention strategies will also be discussed.
    Source

    Curr Opin Virol. 2016 Oct;20:78-84. doi: 10.1016/j.coviro.2016.09.006. Epub 2016 Sep 27. Link to article on publisher's site

    DOI
    10.1016/j.coviro.2016.09.006
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/50520
    PubMed ID
    27689909
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    ae974a485f413a2113503eed53cd6c53
    10.1016/j.coviro.2016.09.006
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