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Characterization of cell-death pathways in Punta Toro virus-induced hepatocyte injury

Fangling Xu1, Xiaodong Liang1, Robert B Tesh1

  • 1Department of Pathology and Center for Biodefense & Emerging Infectious Diseases, University of Texas Medical Branch, Galveston, TX, USA.

The Journal of General Virology
|August 30, 2008
PubMed

Insights

Punta Toro virus induces liver cell death through apoptosis. Caspase inhibitors and tumor necrosis factor (TNF) influence this process, indicating complex interactions in viral-induced apoptosis.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Punta Toro virus (PTV) is a Phlebovirus that causes apoptosis in hepatocytes.
  • Apoptosis-related gene expression, including tumor necrosis factor-alpha (TNF-alpha) and its receptors, is altered during PTV infection.
  • The extrinsic and intrinsic pathways of apoptosis are implicated in PTV-induced cell death.

Purpose of the Study:

  • To investigate the roles of the TNF receptor-related extrinsic pathway and the Bcl-2 family-associated mitochondrial pathway in PTV-induced hepatocyte apoptosis.
  • To examine the effects of caspase inhibitors (caspIs) and TNF on cellular viability, viral replication, and apoptotic changes in HepG2 cells infected with PTV.

Main Methods:

  • HepG2 cells were infected with Punta Toro virus (Adames strain).
  • The effects of caspase inhibitors and TNF on cellular viability, viral replication, and apoptosis markers were assessed at various time points.
  • Apoptotic gene expression, caspase activities, and DNA fragmentation were analyzed.

Main Results:

  • Caspase inhibitors reduced PTV-induced cell death, viral load, and apoptotic markers.
  • TNF treatment exacerbated PTV-induced cell death and apoptosis, an effect partially mitigated by caspase inhibitors.
  • PTV infection alters apoptotic gene expression and caspase activity.

Conclusions:

  • Tumor necrosis factor (TNF), caspase-8, and caspase-9 are involved in PTV-induced hepatocytic apoptosis.
  • Additional, potentially interconnected, mediators likely contribute to PTV-induced cell death.
  • Understanding these pathways is crucial for comprehending PTV pathogenesis.

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