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    Host genetic risk factors for West Nile virus infection and disease progression

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    Authors
    Bigham, Abigail W.
    Buckingham, Kati J.
    Husain, Sofia
    Edmond, Mary J.
    Bofferding, Kathryn M.
    Gildersleeve, Heidi
    Rutherford, Ann
    Astakhova, Natalia M.
    Perelygin, Andrey A.
    Busch, Michael P.
    Murray, Kristy O.
    Sejvar, James J.
    Green, Sharone
    Kriesel, John
    Brinton, Margo A.
    Bamshad, Michael
    Show allShow less
    UMass Chan Affiliations
    Department of Medicine, Division of Infectious Diseases and Immunology
    Document Type
    Journal Article
    Publication Date
    2011-09-15
    Keywords
    2',5'-Oligoadenylate Synthetase
    Female
    GTP-Binding Proteins
    Genetic Predisposition to Disease
    Haplotypes
    Humans
    Interferon Regulatory Factor-3
    Male
    Middle Aged
    Polymorphism, Single Nucleotide
    West Nile Fever
    Life Sciences
    Medicine and Health Sciences
    Viruses
    Women's Studies
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    Abstract
    West Nile virus (WNV), a category B pathogen endemic in parts of Africa, Asia and Europe, emerged in North America in 1999, and spread rapidly across the continental U.S. Outcomes of infection with WNV range from asymptomatic to severe neuroinvasive disease manifested as encephalitis, paralysis, and/or death. Neuroinvasive WNV disease occurs in less than one percent of cases, and although host genetic factors are thought to influence risk for symptomatic disease, the identity of these factors remains largely unknown. We tested 360 common haplotype tagging and/or functional SNPs in 86 genes that encode key regulators of immune function in 753 individuals infected with WNV including: 422 symptomatic WNV cases and 331 cases with asymptomatic infections. After applying a Bonferroni correction for multiple tests and controlling for population stratification, SNPs in IRF3 (OR 0.54, p = 0.035) and MX1, (OR 0.19, p = 0.014) were associated with symptomatic WNV infection and a single SNP in OAS1 (OR 9.79, p = 0.003) was associated with increased risk for West Nile encephalitis and paralysis (WNE/P). Together, these results suggest that genetic variation in the interferon response pathway is associated with both risk for symptomatic WNV infection and WNV disease progression.
    Source

    PLoS One. 2011;6(9):e24745. Epub 2011 Sep 15. Link to article on publisher's site

    DOI
    10.1371/journal.pone.0024745
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/50985
    PubMed ID
    21935451
    Related Resources

    Link to Article in PubMed

    Rights
    This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.
    ae974a485f413a2113503eed53cd6c53
    10.1371/journal.pone.0024745
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