Abstract
Response to IFN involves a rapid and direct signal transduction mechanism that quickly reports that presence of extracellular cytokine to the cell nucleus, preserving the specificity inherent in cytokine-receptor interactions to transcriptionally induce expression of a set of genes encoding important antiviral proteins. Establishment of the resulting antiviral state provides a crucial initial line of defense against viral infection. Studies of IFN-deficient cells and animals derived by gene targeting have demonstrated the essential nature of IFN-mediated innate immunity. The long co-evolutionary history of viruses with their hosts has seen the development of a variety of evasive adaptations that allow viruses to circumvent or inactivate host antiviral mechanisms. Further understanding of both host and viral components of this battle may provide important new strategies for vaccine development and creation of novel antiviral compounds.
Publication types
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Antiviral Agents / antagonists & inhibitors
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Antiviral Agents / immunology*
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Antiviral Agents / metabolism
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism
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Gene Expression Regulation
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Humans
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Interferons / antagonists & inhibitors
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Interferons / biosynthesis
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Interferons / immunology*
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Janus Kinase 1
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Mice
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Protein-Tyrosine Kinases / metabolism
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RNA, Double-Stranded / metabolism
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Receptors, Interferon / metabolism
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STAT1 Transcription Factor
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Signal Transduction
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Trans-Activators / genetics
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Trans-Activators / metabolism
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Viruses / immunology*
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Viruses / pathogenicity
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eIF-2 Kinase / metabolism
Substances
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Antiviral Agents
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DNA-Binding Proteins
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RNA, Double-Stranded
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Receptors, Interferon
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STAT1 Transcription Factor
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STAT1 protein, human
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Stat1 protein, mouse
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Trans-Activators
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Interferons
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Protein-Tyrosine Kinases
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JAK1 protein, human
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Jak1 protein, mouse
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Janus Kinase 1
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eIF-2 Kinase