Abstract
Influenza viruses lacking the interferon (IFN)-antagonistic non-structural NS1 protein are strongly attenuated. Here, we show that mutants of a highly virulent variant of A/PR/8/34 (H1N1) carrying either a complete deletion or C-terminal truncations of NS1 were far more potent inducers of IFN in infected mice than NS1 mutants derived from standard A/PR/8/34. Efficient induction of IFN correlated with successful initial virus replication in mouse lungs, indicating that the IFN response is boosted by enhanced viral activity. As the new NS1 mutants can be handled in standard biosafety laboratories, they represent convenient novel tools for studying virus-induced IFN expression in vivo.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Gene Deletion*
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Humans
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Influenza A Virus, H1N1 Subtype* / genetics
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Influenza A Virus, H1N1 Subtype* / immunology
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Influenza A Virus, H1N1 Subtype* / pathogenicity
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Interferon-beta / antagonists & inhibitors
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Interferon-beta / metabolism*
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Lung / virology
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Mice
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Mice, Inbred BALB C
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Mutation
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Orthomyxoviridae Infections / immunology*
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Orthomyxoviridae Infections / physiopathology
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Orthomyxoviridae Infections / virology
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Viral Nonstructural Proteins / genetics*
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Viral Nonstructural Proteins / metabolism
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Virulence
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Virus Replication
Substances
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INS1 protein, influenza virus
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Viral Nonstructural Proteins
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Interferon-beta