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Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists.

Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists. Research Abstract Details 

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  • Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists. Abstract Text:

    sarah a kopecky-brombergSarah A Kopecky-Bromberg,luis Luis ,matthew friemanMatthew Frieman,ralph a baricRalph A Baric,peter palesePeter Palese,

    The severe acute respiratory syndrome coronavirus (SARS-CoV) is highly pathogenic in humans, with a death rate near 10%. This high pathogenicity suggests that SARS-CoV has developed mechanisms to overcome the host innate immune response. It has now been determined that SARS-CoV open reading frame (ORF) 3b, ORF 6, and N proteins antagonize interferon, a key component of the innate immune response. All three proteins inhibit the expression of beta interferon (IFN-beta), and further examination revealed that these SARS-CoV proteins inhibit a key protein necessary for the expression of IFN-beta, IRF-3. N protein dramatically inhibited expression from an NF-kappaB-responsive promoter. All three proteins were able to inhibit expression from an interferon-stimulated response element (ISRE) promoter after infection with Sendai virus, while only ORF 3b and ORF 6 proteins were able to inhibit expression from the ISRE promoter after treatment with interferon. This indicates that N protein inhibits only the synthesis of interferon, while ORF 3b and ORF 6 proteins inhibit both interferon synthesis and signaling. ORF 6 protein, but not ORF 3b or N protein, inhibited nuclear translocation but not phosphorylation of STAT1. Thus, it appears that these three interferon antagonists of SARS-CoV inhibit the interferon response by different mechanisms.

    Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists. Publishing Authors By Initials

    sa kopecky-brombergSA Kopecky-Bromberg,l L ,m friemanM Frieman,ra baricRA Baric,p paleseP Palese,

    For similar proteins: viral proteins research abstracts see: proteins: viral proteins research

    PUBMED ID PMID:

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    Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: Journal of virology

    VOLUME: 81

    Page Numbers: 548-57

    Journal Abbreviation: J. Virol.

    ISSN: 0022-538X

    DAY: 15

    MONTH: 11

    YEAR: 2006

    Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 113724

    Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists. Keywords Mesh Terms:

    KEYWORDS: Viral Proteins

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists. Information

    Substance Name: Interferon-beta

    Registry Number: 77238-31-4

    Grant and Affiliation Information for Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists.

    AFFILIATION: Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029-6574, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States PHS

    GRANT: T32 A1007645

    ACRONYM: AI

    MEDLINETA: J Virol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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