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    Severe acute respiratory syndrome coronavirus ORF7a inhibits bone marrow stromal antigen 2 virion tethering through a novel mechanism of glycosylation interference

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    Author
    Taylor, J.K.
    Coleman, C.M.
    Postel, S.
    Sisk, J.M.
    Venkataraman, T.
    Sundberg, E.J.
    Frieman, M.B.
    Date
    2015
    Journal
    Journal of Virology
    Publisher
    American Society for Microbiology
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1128/JVI.02274-15
    Abstract
    Severe acute respiratory syndrome (SARS) emerged in November 2002 as a case of atypical pneumonia in China, and the causative agent of SARS was identified to be a novel coronavirus, severe acute respiratory syndrome coronavirus (SARS-CoV). Bone marrow stromal antigen 2 (BST-2; also known as CD317 or tetherin) was initially identified to be a pre-B-cell growth promoter, but it also inhibits the release of virions of the retrovirus human immunodeficiency virus type 1 (HIV-1) by tethering budding virions to the host cell membrane. Further work has shown that BST-2 restricts the release of many other viruses, including the human coronavirus 229E (hCoV-229E), and the genomes of many of these viruses encode BST-2 antagonists to overcome BST-2 restriction. Given the previous studies on BST-2, we aimed to determine if BST-2 has the ability to restrict SARS-CoV and if the SARS-CoV genome encodes any proteins that modulate BST-2's antiviral function. Through an in vitro screen, we identified four potential BST-2 modulators encoded by the SARS-CoV genome: the papain-like protease (PLPro), nonstructural protein 1 (nsp1), ORF6, and ORF7a. As the function of ORF7a in SARS-CoV replication was previously unknown, we focused our study on ORF7a. We found that BST-2 does restrict SARS-CoV, but the loss of ORF7a leads to a much greater restriction, confirming the role of ORF7a as an inhibitor of BST-2. We further characterized the mechanism of BST-2 inhibition by ORF7a and found that ORF7a localization changes when BST-2 is overexpressed and ORF7a binds directly to BST-2. Finally, we also show that SARSCoV ORF7a blocks the restriction activity of BST-2 by blocking the glycosylation of BST-2.
    Sponsors
    National Institute of Allergy and Infectious Diseases, NIAID: R01AI087452; National Institute of Allergy and Infectious Diseases, NIAID: RO1AI1095569
    Keyword
    SARS-CoV
    SARSCoV ORF7a
    SARS Virus
    Coronavirus Infections
    Bone Marrow Stromal Antigen 2
    Virion
    Glycosylation
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-84949652761&doi=10.1128%2fJVI.02274-15&partnerID=40&md5=8d733fa8a44c12c40ad0bf2aca7bcf1a; http://hdl.handle.net/10713/12408
    ae974a485f413a2113503eed53cd6c53
    10.1128/JVI.02274-15
    Scopus Count
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    UMB Coronavirus Publications

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