Abstract
Severe acute respiratory syndrome (SARS) is characterized by rapidly progressing respiratory failure resembling acute/adult respiratory distress syndrome (ARDS) associated with uncontrolled inflammatory responses. Here, we demonstrated that, among five accessory proteins of SARS coronavirus (SARS-CoV) tested, 3a/X1 and 7a/X4 were capable of activating nuclear factor kappa B (NF-kappaB) and c-Jun N-terminal kinase (JNK), and significantly enhanced interleukin 8 (IL-8) promoter activity. Furthermore, 3a/X1 and 7a/X4 expression in A549 cells enhanced production of inflammatory chemokines that were known to be up-regulated in SARS-CoV infection. Our results suggest potential involvement of 3a/X1 and 7a/X4 proteins in the pathological inflammatory responses in SARS.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Line
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Chemokines / biosynthesis*
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Enzyme Activation
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Gene Expression
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Humans
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JNK Mitogen-Activated Protein Kinases / metabolism
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NF-kappa B / metabolism*
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Promoter Regions, Genetic / genetics
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Severe acute respiratory syndrome-related coronavirus / genetics
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Severe acute respiratory syndrome-related coronavirus / metabolism*
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Viral Matrix Proteins / genetics
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Viral Matrix Proteins / metabolism*
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Viral Proteins / genetics
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Viral Proteins / metabolism*
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Viral Structural Proteins / genetics
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Viral Structural Proteins / metabolism*
Substances
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Chemokines
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NF-kappa B
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ORF3A protein, SARS coronavirus
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Viral Matrix Proteins
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Viral Proteins
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Viral Structural Proteins
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sars7a protein, SARS virus
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JNK Mitogen-Activated Protein Kinases