Abstract
Mx+ mice are much more resistant to influenza virus than Mx- strains. The resistance is mediated by interferon (IFN) alpha/beta. After IFN treatment, Mx+ but not Mx- cells accumulate Mx protein and become specifically resistant to orthomyxoviruses. cDNA encoding Mx protein was cloned and sequenced. Southern analyses indicate that Mx- alleles derive from their Mx+ counterpart by deletions. IFN-treated Mx+ cells contained a 3.5 kb Mx mRNA, while Mx- cells showed only traces of shorter Mx RNA. Mx- cells transformed with Mx cDNA expressed Mx protein constitutively to varying extents; resistance of individual cells to influenza virus correlated with Mx protein expression. Thus, specific resistance to influenza virus in vivo may be attributed to Mx protein expression and is independent of other IFN-mediated effects.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Animals
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Base Sequence
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Cell Line
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Chromosome Deletion
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DNA / genetics
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Fibroblasts
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GTP-Binding Proteins*
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Gene Expression Regulation / drug effects
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Immunity, Innate
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Influenza A virus / physiology*
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Interferon Type I / pharmacology
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Interferon Type I / physiology
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Mice
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Mice, Inbred A / genetics
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Mice, Inbred BALB C
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Mice, Mutant Strains / genetics
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Myxovirus Resistance Proteins
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Protein Biosynthesis
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Proteins / genetics
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Proteins / physiology*
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RNA, Messenger / genetics
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RNA, Messenger / isolation & purification
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Transformation, Genetic
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Vesicular stomatitis Indiana virus / physiology
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Virus Replication
Substances
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Interferon Type I
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Mx1 protein, mouse
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Myxovirus Resistance Proteins
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Proteins
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RNA, Messenger
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DNA
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GTP-Binding Proteins
Associated data
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GENBANK/M12279
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GENBANK/M21037