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Gene expression profiling by microarray analysis reveals an important role for caspase-1 in dengue virus-induced

A M A Nasirudeen1, Ding Xiang Liu

  • 1Institute of Molecular and Cell Biology, Proteos, Singapore, Singapore.

Journal of Medical Virology
|April 22, 2009
PubMed

Insights

Dengue virus infection triggers apoptosis via p53 and mitochondria. Caspase-1 activation significantly contributes to this cell death, offering a potential therapeutic target for dengue.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Dengue virus infection is known to induce apoptosis in host cells.
  • Previous studies implicated p53 and mitochondrial pathways in this process.
  • The precise molecular mechanisms require further elucidation.

Purpose of the Study:

  • To investigate the gene expression profiles of dengue virus-infected cells with varying p53 status.
  • To identify key cellular pathways and genes involved in dengue virus-induced apoptosis.
  • To explore the role of caspase-1 in dengue virus-induced cell death.

Main Methods:

  • Utilized p53-deficient (H1299) and p53-knockin (H273) cell lines infected with dengue type 1 virus.
  • Analyzed mRNA expression profiles using Affymetrix array analysis.
  • Confirmed gene expression changes via qualitative and quantitative PCR, including gene silencing and enzyme inhibition experiments.

Main Results:

  • Identified 183 upregulated genes in dengue virus-infected cells.
  • Observed significant upregulation of interferon (IFN) pathway, cell cycle, signal transduction, and ubiquitin-proteasome pathway genes.
  • Demonstrated a 32-fold increase in caspase-1 expression in p53-knockin cells; caspase-1 inhibition reduced apoptosis.

Conclusions:

  • Dengue virus infection profoundly alters cellular gene expression, impacting key biological pathways.
  • Caspase-1 plays a critical role in mediating dengue virus-induced apoptosis.
  • Targeting caspase-1 may represent a viable strategy to mitigate dengue virus-induced cell death.

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