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Visna/maedi virus-induced apoptosis involves the intrinsic mitochondrial pathway

V Bellet1, S Delebassée, C Bosgiraud

  • 1Laboratoire de Microbiologie, Faculté de Pharmacie, Limoges, France.

Archives of Virology
|June 29, 2004
PubMed

Insights

Visna/maedi virus (VMV) infection triggers apoptosis in sheep cells via the intrinsic mitochondrial pathway. This process involves p53 activation and mitochondrial damage, leading to programmed cell death.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Visna/maedi virus (VMV) is a pathogen affecting sheep.
  • Apoptosis, or programmed cell death, is a critical cellular process.
  • The intrinsic apoptotic pathway involves mitochondria and is often regulated by p53.

Purpose of the Study:

  • To investigate the mechanism of VMV-induced apoptosis in sheep choroid plexus cells.
  • To determine the role of the intrinsic mitochondrial pathway in VMV infection.
  • To examine the involvement of the p53 pathway in VMV-induced apoptosis.

Main Methods:

  • Sheep choroid plexus cells were infected with VMV.
  • Mitochondrial potential was assessed using JC-1 staining.
  • Apoptosis Inducing Factor and cytochrome c release were measured.
  • p53, p21, and bcl-2 expression levels were analyzed.
  • DNA flow cytometry was used to detect apoptotic populations.

Main Results:

  • VMV infection induced apoptosis in sheep choroid plexus cells.
  • Mitochondrial membrane permeabilization and cytochrome c release were observed.
  • Apoptosis Inducing Factor translocated to the nucleus.
  • The p53 pathway was activated, leading to bcl-2 downregulation.
  • Increased p21 expression occurred without cell cycle arrest.

Conclusions:

  • VMV-induced apoptosis in sheep cells is mediated by the intrinsic mitochondrial pathway.
  • p53 activation plays a significant role in this apoptotic process.
  • Mitochondrial integrity is compromised during VMV infection, leading to cell death.

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