Abstract
Mouse hepatitis virus (MHV) does not induce interferon (IFN) production in fibroblasts or bone marrow-derived dendritic cells. In this report, we show that the essential IFN-beta transcription factors NF-kappaB and IFN regulatory factor 3 are not activated for nuclear translocation and gene induction during infection. However, MHV was unable to inhibit the activation of these factors and subsequent IFN-beta production induced by poly(I:C). Further, MHV infection did not inhibit IFN-beta production mediated by known host pattern recognition receptors (PRRs) (RIG-I, Mda-5, and TLR3). These results are consistent with the notion that double-stranded RNA, produced during MHV infection, is not accessible to cellular PRRs.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Cell Line
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DEAD-box RNA Helicases / genetics
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DEAD-box RNA Helicases / metabolism
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Gene Expression Regulation
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Humans
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Interferon Regulatory Factor-3 / genetics
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Interferon Regulatory Factor-3 / metabolism
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Interferon-Induced Helicase, IFIH1
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Interferon-beta / biosynthesis*
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Membrane Proteins / genetics
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Membrane Proteins / metabolism
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Mice
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Murine hepatitis virus / classification
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Murine hepatitis virus / immunology
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Murine hepatitis virus / pathogenicity*
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NF-kappa B / genetics
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NF-kappa B / metabolism
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / metabolism
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Poly I-C / pharmacology
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RNA, Double-Stranded / genetics
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RNA, Double-Stranded / immunology*
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RNA, Double-Stranded / metabolism
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Receptors, Cell Surface
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Toll-Like Receptor 3 / genetics
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Toll-Like Receptor 3 / metabolism
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Transcriptional Activation
Substances
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Interferon Regulatory Factor-3
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Membrane Proteins
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NF-kappa B
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Nerve Tissue Proteins
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RNA, Double-Stranded
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Receptors, Cell Surface
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Robo3 protein, mouse
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Toll-Like Receptor 3
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Interferon-beta
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Ifih1 protein, mouse
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DEAD-box RNA Helicases
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Interferon-Induced Helicase, IFIH1
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Poly I-C