1. Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis
- Author
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Shi-Yi Shiu, Kuan-Hsun Lin, Cheng Wen Lin, Tsung-Han Hsieh, and Jeng-Yi Li
- Subjects
Microbiology (medical) ,Programmed cell death ,viruses ,Immunology ,Caspase 3 ,Biology ,Severe Acute Respiratory Syndrome ,Transfection ,medicine.disease_cause ,Microbiology ,Cell Line ,Promonocyte ,Pathogenesis ,Viral Proteins ,medicine ,Humans ,Immunology and Allergy ,Annexin A5 ,skin and connective tissue diseases ,Research Articles ,Coronavirus ,reactive oxygen species ,chemistry.chemical_classification ,Reactive oxygen species ,nuclear factor-kappa B signalling ,Rhodamines ,Activator (genetics) ,apoptosis ,3C Viral Proteases ,NF-kappa B ,3CLpro ,General Medicine ,Molecular biology ,Caspase 9 ,Transcription Factor AP-1 ,Cysteine Endopeptidases ,Infectious Diseases ,SARS-coronavirus ,Microscopy, Fluorescence ,Severe acute respiratory syndrome-related coronavirus ,chemistry ,Apoptosis ,Caspases ,Signal Transduction - 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.
- Published
- 2006
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