Abstract
The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS-CoV has been demonstrated to induce cell apoptosis in Vero-E6 cells. The possible role of SARS-CoV 3C-like protease (3CLpro) in virus-induced apoptosis is characterized in this study. Growth arrest and apoptosis via caspase-3 and caspase-9 activities were demonstrated in SARS-CoV 3CLpro -expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS-CoV 3CLpro -expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CLpro increased the activation of the nuclear factor-kappa B-dependent reporter, but inhibited activator protein-1-dependent transcription. This finding is likely to be responsible for virus-induced apoptotic signalling.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3C Viral Proteases
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Annexin A5 / chemistry
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Apoptosis / immunology*
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Caspase 3
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Caspase 9
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Caspases / metabolism
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Cell Line
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Cysteine Endopeptidases / biosynthesis
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Cysteine Endopeptidases / genetics
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Cysteine Endopeptidases / immunology*
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Humans
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Microscopy, Fluorescence
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NF-kappa B / immunology
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Reactive Oxygen Species / metabolism
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Rhodamines / chemistry
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Severe Acute Respiratory Syndrome / virology
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Severe acute respiratory syndrome-related coronavirus / enzymology*
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Severe acute respiratory syndrome-related coronavirus / genetics
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Severe acute respiratory syndrome-related coronavirus / immunology
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Signal Transduction
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Transcription Factor AP-1 / immunology
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Transfection
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Viral Proteins / biosynthesis
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Viral Proteins / genetics
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Viral Proteins / immunology*
Substances
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Annexin A5
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NF-kappa B
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Reactive Oxygen Species
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Rhodamines
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Transcription Factor AP-1
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Viral Proteins
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dihydrorhodamine 123
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CASP3 protein, human
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CASP9 protein, human
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Caspase 3
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Caspase 9
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Caspases
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Cysteine Endopeptidases
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3C Viral Proteases