Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3

Lui, Pak-Yin; Wong, Lok-Yin Roy; Fung, Cheuk-Lai; Siu, Kam‐Leung; Yeung, Man Lung; Yuen, Kit‐San; Chan, Chi-Ping; Woo, Patrick C. Y.; Yuen, Kwok‐Yung; Jin, Dong Yan

doi:10.1038/emi.2016.33

Cited by 118 publications

(156 citation statements)

References 59 publications

(97 reference statements)

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“…Z. Zhou, et al Virus Research 278 (2020) 197843 phosphorylation by the membrane protein, the middle east respiratory syndrome coronavirus (MERS-CoV) could suppress the type I interferon expression (Lui et al, 2016). The nonstructural protein (NSP) 5 encoded by PDCoV inhibited IFN-β production through the cleavage of NEMO, which was responsible for the recruitment of TBK1 and IKKε and the activation of IKK complex (Zhu et al, 2017b).…”

Section: Discussionmentioning

confidence: 99%

Swine acute diarrhea syndrome coronavirus (SADS-CoV) antagonizes interferon-β production via blocking IPS-1 and RIG-I

et al. 2020

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A B S T R A C TSwine acute diarrhea syndrome coronavirus (SADS-CoV), a newly emerging enteric coronavirus, is considered to be associated with swine acute diarrhea syndrome (SADS) which has caused significantly economic losses to the porcine industry. Interactions between SADS-CoV and the host innate immune response is unclear yet. In this study, we used IPEC-J2 cells as a model to explore potential evasion strategies employed by SADS-CoV. Our results showed that SADS-CoV infection failed to induce IFN-β production, and inhibited poly (I:C) and Sendai virus (SeV)-triggered IFN-β expression. SADS-CoV also blocked poly (I:C)-induced phosphorylation and nuclear translocation of IRF-3 and NF-κB. Furthermore, SADS-CoV did not interfere with the activity of IFN-β promoter stimulated by IRF3, TBK1 and IKKε, but counteracted its activation induced by IPS-1 and RIG-I. Collectively, this study is the first investigation that shows interactions between SADS-CoV and the host innate immunity, which provides information of the molecular mechanisms underlying SASD-CoV infection.

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Section: Discussionmentioning

confidence: 99%

Swine acute diarrhea syndrome coronavirus (SADS-CoV) antagonizes interferon-β production via blocking IPS-1 and RIG-I

et al. 2020

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“…MERS‐CoV M protein is capable of differentially suppressing the RIG‐I‐induced activation of IRF3. M protein interacts with TRAF3 and disrupts TRAF3–TBK1 association, leading to reduced activation of IRF3 (Lui et al, ). TRAF3 functions as an adapter that bridges the mitochondrial transducer MAVS with the downstream signaling complex containing TBK1 and IKK‐ɛ kinases that are essential for IRF3 activation (Guo & Cheng, ).…”

Section: Innate Immunementioning

confidence: 99%

Modulation of the immune response by Middle East respiratory syndrome coronavirus

Shokri

Mahmoudvand

Taherkhani

et al. 2018

Journal Cellular Physiology

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Coronavirus (CoV) infections are commonly associated with respiratory and enteric disease in humans and animals. In 2012, a new human disease called Middle East respiratory syndrome (MERS) emerged in the Middle East. MERS was caused by a virus that was originally called human coronavirus-Erasmus Medical Center/2012 but was later renamed as Middle East respiratory syndrome coronavirus (MERS-CoV). MERS-CoV causes high fever, cough, acute respiratory tract infection, and multiorgan dysfunction that may eventually lead to the death of the infected individuals. The exact origin of MERS-CoV remains unknown, but the transmission pattern and evidence from virological studies suggest that dromedary camels are the major reservoir host, from which human infections may sporadically occur through the zoonotic transmission. Human to human transmission also occurs in healthcare facilities and communities. Recent studies on Middle Eastern respiratory continue to highlight the need for further understanding the virus-host interactions that govern disease severity and infection outcome. In this review, we have highlighted the major mechanisms of immune evasion strategies of MERS-CoV. We have demonstrated that M, 4a, 4b proteins and Plppro of MERS-CoV inhibit the type I interferon (IFN) and nuclear factor-κB signaling pathways and therefore facilitate innate immune evasion. In addition, nonstructural protein 4a (NSP4a), NSP4b, and NSP15 inhibit double-stranded RNA sensors. Therefore, the mentioned proteins limit early induction of IFN and cause rapid apoptosis of macrophages. MERS-CoV strongly inhibits the activation of T cells with downregulation of antigen presentation. In addition, uncontrolled secretion of interferon ɣ-induced protein 10 and monocyte chemoattractant protein-1 can suppress proliferation of human myeloid progenitor cells.

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“…The mechanism of inhibition of type I IFN response by IFNβ has been closely investigated in several viruses. For example, in TGEV, PEDV, murine hepatitis virus, severe acute respiratory syndrome (SARS)-CoV, and middle east respiratory syndrome (MERS)-CoV, it has been reported that structural proteins, excluding non-structural proteins and spike protein, inhibit IFNβ production (Case et al, 2018(Case et al, , 2016Ding et al, 2017;Hu et al, 2017;Li et al, 2016;Lu et al, 2011;Lui et al, 2016;Zhang et al, 2016). However, it is unclear whether type I IFN responses are inhibited by FCoV.…”

Section: Introductionmentioning

confidence: 99%

Differential induction of type I interferon by type I and type II feline coronaviruses in vitro

Doki

Yabe

Takano

et al. 2018

Research in Veterinary Science

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A B S T R A C TFeline infectious peritonitis (FIP) is a feline coronavirus (FCoV)-induced fatal disease in wild and domestic cats. There are two FCoV serotypes. Both type I and II FCoV can replicate in Felis catus whole fetus (fcwf)-4 cells, but the replicability of type I FCoV in feline cell lines is lower than that of type II FCoV, the reason for which is unclear. Inhibition of IFNβ production by non-structural and structural proteins, excluding spike protein has been reported in many coronavirus infections. In this study, we investigated whether IFNβ is involved in the difference in replicability in feline cell lines between types I and II FCoV. When fcwf-4 cells were infected with FCoV, the virus titer of type II FCoV in the culture supernatant was higher than that of type I FIPV. When the IFNβ expression level in FCoV-infected fcwf-4 cells was semi-quantitatively analyzed, infection with type I FIPV, excluding type I FIPV UCD-1, highly induced IFNβ expression. In contrast, induction of IFNβ by type II FCoV infection was significantly lower than that by type I FIPV. In addition, when fcwf-4 cells were adsorbed by FIPV and then stimulated with Poly(I:C), type II FCoV infection inhibited Poly(I:C)-induced IFNβ gene expression. Also, the proliferation of type I FIPV was enhanced by a IFN inhibitor. These findings clarified that, unlike type I FIPV, type II FCoV strongly inhibits IFNβ expression in infected cells. It was also suggested that the IFNβ-inducing ability is different among type I FIPV strains.

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Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3

Cited by 118 publications

References 59 publications

Swine acute diarrhea syndrome coronavirus (SADS-CoV) antagonizes interferon-β production via blocking IPS-1 and RIG-I

Swine acute diarrhea syndrome coronavirus (SADS-CoV) antagonizes interferon-β production via blocking IPS-1 and RIG-I

Modulation of the immune response by Middle East respiratory syndrome coronavirus

Differential induction of type I interferon by type I and type II feline coronaviruses in vitro

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