Related Experiment Video
Updated: Aug 15, 2026
Modelling Zika Virus Infection of the Developing Human Brain In Vitro Using Stem Cell Derived Cerebral Organoids
Published on: September 19, 2017
Involvement of Fas and FasL in Ectromelia virus-induced apoptosis in mouse brain
Małgorzata Krzyzowska1, Joanna Cymerys, Anna Winnicka
1Division of Virology, Mycology and Immunology, Department of Preclinical Sciences, Ciszewskiego 8, 02-786 Warsaw, Poland. krzyzowska@yahoo.com
Abstract:
In this study we showed that the virulent Moscow strain of Ectromelia virus (ECTV-MOS) infection leads to induction of apoptosis in the BALB/c mouse central nervous system. ECTV-MOS-infected cells and inflammation sites were found in brain parenchyma between 5 and 15 days after footpad infection with ECTV-MOS. Infected cells consisted of microglia and monocytes, astrocytes and oligodendrocytes and these type of cells underwent apoptosis within 5-15 days post infection (d.p.i.). The highest number of apoptotic cells was found at 5 and 10 d.p.i. and represented mainly microglia (61.4% and 38.6% of apoptotic cells, respectively) and astrocytes (21% and 8.9%, respectively). The number of apoptotic oligodendrocytes was 5.4% and 4.5%, respectively. Fluorometric assays demonstrated involvement of caspase-1, -3 and -8 but not caspase-9 in apoptosis in ECTV-MOS-infected mouse brains. Expression of Fas/FasL was significantly increased on ECTV-MOS-infected cells between 5 and 15 d.p.i., whereas Fas was up-regulated also on the surrounding, non-infected cells. Taking together we may conclude that ECTV-MOS infection of microglia and astrocytes leads to local inflammation resulting in Fas/FasL up-regulation and apoptosis, which limits mouse central nervous system infection with ECTV-MOS.
Insights
Ectromelia virus (ECTV-MOS) infection induces apoptosis in mouse brain cells, primarily microglia and astrocytes, between 5-15 days post-infection. This programmed cell death, involving specific caspases and Fas/FasL, helps limit central nervous system infection.
Area of Science:
- Neurovirology
- Immunology
- Cell Biology
Background:
- Ectromelia virus (ECTV) causes mousepox, a potentially lethal disease.
- The central nervous system (CNS) can be a target for viral infections, leading to severe neurological complications.
Purpose of the Study:
- To investigate the induction of apoptosis in the BALB/c mouse CNS following ECTV-MOS infection.
- To identify the specific cell types undergoing apoptosis and the molecular mechanisms involved.
Main Methods:
- Footpad infection of BALB/c mice with ECTV-MOS.
- Histological analysis of brain tissue at various time points post-infection (5-15 days).
- Fluorometric assays to detect caspase activity and assessment of Fas/FasL expression.
Main Results:
- ECTV-MOS infection led to apoptosis in microglia, monocytes, astrocytes, and oligodendrocytes within the mouse brain parenchyma.
- Microglia and astrocytes were the predominant cell types undergoing apoptosis, peaking at 5 and 10 days post-infection.
- Apoptosis involved caspase-1, -3, and -8, but not caspase-9, and was associated with increased Fas/FasL expression on infected and surrounding cells.
Conclusions:
- ECTV-MOS infection triggers apoptosis in CNS cells, particularly microglia and astrocytes.
- The observed apoptosis, mediated by caspases and Fas/FasL pathway, plays a role in limiting viral spread within the mouse CNS.
More Related Videos
08:22A Novel Strategy Combining Array-CGH, Whole-exome Sequencing and In Utero Electroporation in Rodents to Identify Causative Genes for Brain Malformations
Published on: December 1, 2017
08:20Analysis of Apoptosis in Zebrafish Embryos by Whole-mount Immunofluorescence to Detect Activated Caspase 3
Published on: December 20, 2013