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Bluetongue virus infection: activation of the MAP kinase-dependent pathway is required for apoptosis

Eduardo Mortola1, Alejandra Larsen

  • 1Inmunología Veterinaria, Facultad de Cs. Veterinarias, Universidad Nacional de La Plata, 60 y 118, 1900 La Plata, Argentina. mortola@fcv.unlp.edu.ar

Research in Veterinary Science
|May 4, 2010
PubMed

Insights

Bluetongue virus (BTV) infection triggers apoptosis in mammalian cells via mitogen-activated protein kinases (MAPKs). Inhibiting c-Jun N-terminal kinases (JNKs) and p38 MAPK reduces apoptosis, highlighting their role in BTV pathophysiology.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Bluetongue virus (BTV) is a double-stranded RNA virus known to induce apoptosis in mammalian cells.
  • Mitogen-activated protein kinases (MAPKs) are recognized mediators of apoptosis.
  • Previous studies established the involvement of mitochondrial apoptotic pathways and NF-κB activation in BTV-induced apoptosis.

Purpose of the Study:

  • To investigate the role of MAPK signaling pathways in BTV-induced apoptosis.
  • To determine which specific MAPKs are activated during BTV infection and contribute to cell death.

Main Methods:

  • Mammalian cell cultures were infected with BTV.
  • Mitogen-activated protein kinase (MAPK) activation was assessed post-infection.
  • Specific MAPK inhibitors (JNK, p38, ERK) were used to evaluate their effect on apoptosis induction.
  • Mitochondrial release of cytochrome c and caspase 3 activation were measured.

Main Results:

  • BTV infection led to the activation of MAPKs, including JNK and p38.
  • Pre-treatment with JNK and p38 MAPK inhibitors significantly reduced BTV-induced apoptosis.
  • Extracellular signal-related kinase (ERK) activation did not appear to play a significant role in BTV-induced apoptosis.
  • JNK and p38 activation were found to regulate cytochrome c release and caspase 3 activation.

Conclusions:

  • MAPK signaling, specifically JNK and p38 pathways, is crucial for BTV-induced apoptosis in mammalian cells.
  • These findings elucidate the molecular mechanisms underlying BTV-induced cell death.
  • Understanding MAPK involvement provides insights into BTV pathophysiology and potential therapeutic targets.

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