Abstract
Infection with JHMV results in the transcriptional activation of two host cell genes encoding proinflammatory cytokines, tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta. Analysis of irradiated mice showed that IL-1 beta mRNA accumulation in the central nervous system was predominantly derived from the mononuclear infiltrate. By contrast, accumulation of TNF-alpha mRNA was unaffected by immunosuppression, suggesting that resident cells were the source of this cytokine. Infected mice were treated with anti-TNF antibody to determine if TNF-alpha contributed to either the encephalomyelitis or demyelination associated with JHMV infection. Surprisingly, neither the cellular infiltrate nor demyelination were affected. In vitro analysis showed that IL-1 beta but not TNF was secreted from JHMV infected macrophages. The absence of TNF secretion is due to a block in translation of the TNF mRNA which accumulates during infection.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Brain / immunology
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Brain / virology*
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Cells, Cultured
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Coronavirus Infections / immunology*
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Cytokines / biosynthesis*
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Demyelinating Diseases / immunology
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Demyelinating Diseases / pathology
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Demyelinating Diseases / virology
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Encephalomyelitis / immunology
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Encephalomyelitis / pathology
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Encephalomyelitis / virology
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Gene Expression Regulation, Viral
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Interleukin-1 / biosynthesis*
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Kinetics
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Lipopolysaccharides / pharmacology
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Macrophages, Peritoneal / drug effects
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Macrophages, Peritoneal / immunology*
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Mice
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Mice, Inbred BALB C
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Murine hepatitis virus*
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Protein Biosynthesis*
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RNA, Messenger / analysis
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RNA, Messenger / biosynthesis
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RNA, Messenger / metabolism
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Time Factors
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Transcription, Genetic*
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Tumor Necrosis Factor-alpha / biosynthesis*
Substances
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Cytokines
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Interleukin-1
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Lipopolysaccharides
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RNA, Messenger
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Tumor Necrosis Factor-alpha