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Poliovirus induces Bax-dependent cell death mediated by c-Jun NH2-terminal kinase

Arnaud Autret1, Sandra Martin-Latil, Laurence Mousson

  • 1Biologie des Virus Entériques, Institut Pasteur, 28 rue du Docteur Roux, 75724 Paris cedex 15, France.

Journal of Virology
|May 12, 2007
PubMed

Insights

Poliovirus infection triggers apoptosis in neuronal cells by activating the JNK pathway, leading to Bax activation and mitochondrial damage. This study reveals a key mechanism in poliovirus pathogenesis.

Area of Science:

  • Neuroscience
  • Virology
  • Cell Biology

Background:

  • Poliovirus (PV) causes paralytic poliomyelitis through motor neuron destruction.
  • The precise mechanisms of PV-induced neuronal cell death remain largely unknown.
  • Apoptosis, a programmed cell death process, is implicated in PV-infected mice.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which poliovirus induces apoptosis in neuronal cells.
  • To investigate the role of mitochondria and specific signaling pathways in PV-induced cell death.
  • To identify potential therapeutic targets for poliovirus-induced neuronal damage.

Main Methods:

  • Neuronal IMR5 cells were infected with poliovirus.
  • Mitochondrial outer membrane permeabilization was assessed by cytochrome c release and mitochondrial potential loss.
  • Activation of Bax and c-Jun NH(2)-terminal kinase (JNK) was analyzed.
  • The effects of Bax neutralization (vMIA) and JNK inhibition (SP600125) were evaluated.

Main Results:

  • PV infection induced cytochrome c release and loss of mitochondrial transmembrane potential in IMR5 cells.
  • PV infection activated the proapoptotic protein Bax, causing its translocation to mitochondria.
  • PV infection led to the activation of c-Jun NH(2)-terminal kinase (JNK).
  • Inhibition of JNK or Bax neutralized PV-induced mitochondrial damage and apoptosis.

Conclusions:

  • Poliovirus induces apoptosis in neuronal cells via JNK-mediated activation of Bax.
  • This pathway involves mitochondrial outer membrane permeabilization, cytochrome c release, and loss of mitochondrial potential.
  • This study provides the first evidence of JNK-mediated, Bax-dependent apoptosis in poliovirus-infected cells, offering insights into poliomyelitis pathogenesis.

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