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

Journal of Virology
Sarah A Kopecky-BrombergPeter Palese

Abstract

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 tha...Continue Reading

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Citations

May 12, 2009·Nature Reviews. Microbiology·Stanley Perlman, Jason Netland
Nov 28, 2008·Proceedings of the National Academy of Sciences of the United States of America·Michelle M BeckerMark R Denison
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Mar 7, 2009·Journal of Virology·Yukinobu TohyaShinji Makino
Dec 5, 2008·Microbiology and Molecular Biology Reviews : MMBR·Matthew Frieman, Ralph Baric

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