Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis
| Autor: | Shi-Yi Shiu, Kuan-Hsun Lin, Cheng Wen Lin, Tsung-Han Hsieh, Jeng-Yi Li |
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| Rok vydání: | 2006 |
| Předmět: |
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 |
| Zdroj: | Fems Immunology and Medical Microbiology |
| ISSN: | 1574-695X 0928-8244 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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