Abstract
RNA helicase-like receptors MDA-5 but not RIG-I has been shown to be essential for triggering innate immune responses against picornaviruses. However, virus-host co-evolution has selected for viruses capable of replicating despite host cells antiviral defences. In this report, we demonstrate that RIG-I is degraded during encephalomyocarditis virus (EMCV) infection. This effect is mediated by both the viral-encoded 3C protease and caspase proteinase. In addition, we show that RIG-I overexpression confers IFN-beta promoter activation during EMCV infection, in MDA-5 knockout (MDA-5(-/-)) mouse embryo fibroblasts. This induction is followed by a strong inhibition reflecting the ability of EMCV to disrupt RIG-I signalling. Taken together, our data strongly suggest that during evolution RIG-I has been involved for triggering innate immune response to picornavirus infections.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3C Viral Proteases
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Animals
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Cardiovirus Infections / immunology*
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Cardiovirus Infections / virology
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Caspases / immunology
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Caspases / metabolism
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Cysteine Endopeptidases / immunology
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Cysteine Endopeptidases / metabolism
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DEAD Box Protein 58
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DEAD-box RNA Helicases / immunology
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DEAD-box RNA Helicases / metabolism*
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Encephalomyocarditis virus / immunology*
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Encephalomyocarditis virus / metabolism
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Gene Expression Regulation
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HeLa Cells
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Humans
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Immunity, Innate*
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Interferon-Induced Helicase, IFIH1
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Interferon-beta / immunology*
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Mice
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Promoter Regions, Genetic
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Viral Proteins / immunology
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Viral Proteins / metabolism
Substances
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Viral Proteins
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Interferon-beta
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Caspases
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Cysteine Endopeptidases
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3C Viral Proteases
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Ddx58 protein, mouse
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Ifih1 protein, mouse
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DEAD Box Protein 58
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DEAD-box RNA Helicases
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Interferon-Induced Helicase, IFIH1