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

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.