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Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis

Cheng-Wen Lin1, Kuan-Hsun Lin, Tsung-Han Hsieh

  • 1Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan. cwlin@mail.cmu.edu.tw

FEMS Immunology and Medical Microbiology
|March 24, 2006
PubMed

Insights

Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) 3C-like protease (3CLpro) induces apoptosis by increasing reactive oxygen species and activating NF-kappa B signaling. This protease plays a key role in SARS-CoV-induced cell death.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) pathogenesis is crucial for disease control.
  • SARS-CoV is known to induce apoptosis in host cells.

Purpose of the Study:

  • To investigate the role of SARS-CoV 3C-like protease (3CLpro) in virus-induced apoptosis.
  • To characterize the molecular mechanisms underlying 3CLpro-mediated apoptosis.

Main Methods:

  • Expression of SARS-CoV 3CLpro in human promonocyte cells.
  • Assessing apoptosis via caspase-3 and caspase-9 activity.
  • Measuring reactive oxygen species (ROS) using dihydrorhodamine 123 staining.
  • Analyzing signaling pathways including NF-kappa B and AP-1.

Main Results:

  • SARS-CoV 3CLpro expression induced cell growth arrest and apoptosis.
  • Increased caspase-3 and caspase-9 activities were observed.
  • Elevated levels of cellular reactive oxygen species were detected.
  • 3CLpro activated NF-kappa B-dependent transcription while inhibiting AP-1.

Conclusions:

  • SARS-CoV 3CLpro is implicated in inducing apoptosis.
  • The protease contributes to SARS-CoV pathogenesis through ROS generation and modulation of inflammatory signaling pathways.

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