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dc:abstract "Middle East respiratory syndrome coronavirus (MERS-CoV) infection has claimed hundreds of lives and has become a global threat since its emergence in Saudi Arabia in 2012. The ability of MERS-CoV to evade the host innate antiviral response may contribute to its severe pathogenesis. Many MERS-CoV-encoded proteins were identified to have interferon (IFN)-antagonizing properties, which correlates well with the reduced IFN levels observed in infected patients and ex vivo models. In this study, we fully characterized the IFN-antagonizing property of the MERS-CoV M protein. Expression of MERS-CoV M protein suppressed type I IFN expression in response to Sendai virus infection or poly(I:C) induction. This suppressive effect was found to be specific for the activation of IFN regulatory factor 3 (IRF3) but not nuclear factor-κB. MERS-CoV M protein interacted with TRAF3 and disrupted TRAF3–TBK1 association leading to reduced IRF3 activation. M proteins from MERS-CoV and SARS-CoV have three highly similar conserved N-terminal transmembrane domains and a C-terminal region. Using chimeric and truncation mutants, the N-terminal transmembrane domains of the MERS-CoV M protein were found to be sufficient for its inhibitory effect on IFN expression, whereas the C-terminal domain was unable to induce this suppression. Collectively, our findings suggest a common and conserved mechanism through which highly pathogenic MERS-CoV and SARS-CoV harness their M proteins to suppress type I IFN expression at the level of TBK1-dependent phosphorylation and activation of IRF3 resulting in evasion of the host innate antiviral response." ;
dc:creator "['Lui, Pak-Yin', 'Wong, Lok-Yin Roy', 'Fung, Cheuk-Lai', 'Siu, Kam-Leung', 'Yeung, Man-Lung', 'Yuen, Kit-San', 'Chan, Chi-Ping', 'Woo, Patrick Chiu-Yat', 'Yuen, Kwok-Yung', 'Jin, Dong-Yan']" ;
dc:identifier ,
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dc:issued "2016-01-01"^^xsd:date ;
dc:license "CC BY" ;
dc:title "Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3" ;
sso:has_full_text "True" ;
sso:journal "Emerg Microbes Infect" ;
sso:sha "aa973f2833829b97ebdfd6ce2ac6a29b9100db3a" ;
sso:source_x "PMC" .