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In Vivo Direct Reprogramming of Resident Glial Cells into Interneurons by Intracerebral Injection of Viral Vectors
Published on: June 17, 2019
JC virus induces nonapoptotic cell death of human central nervous system progenitor cell-derived astrocytes
Pankaj Seth1, Frank Diaz, Jung-Hwa Tao-Cheng
1Laboratory of Molecular Medicine and Neuroscience, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.
Abstract:
JC virus (JCV), a human neurotropic polyomavirus, demonstrates a selective glial cell tropism that causes cell death through lytic infection. Whether these cells die via apoptosis or necrosis following infection with JCV remains unclear. To investigate the mechanism of virus-induced cell death, we used a human central nervous system progenitor-derived astrocyte cell culture model developed in our laboratory. Using in situ DNA hybridization, immunocytochemistry, electron microscopy, and an RNase protection assay, we observed that astrocytes support a progressive JCV infection, which eventually leads to nonapoptotic cell death. Infected astrocyte cell cultures showed no difference from noninfected cells in mRNA expression of the caspase family genes or in any ultrastructural features associated with apoptosis. Infected cells demonstrated striking necrotic features such as cytoplasmic vacuolization, watery cytoplasm, and dissolution of organelles. Furthermore, staining for caspase-3 and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling were not detected in infected astrocyte cultures. Our findings suggest that JCV-induced cell death of these progenitor cell-derived astrocytes does not utilize an apoptosis pathway but exhibits a pattern of cell destruction consistent with necrotic cell death.
Insights
John Cunningham virus (JCV) infection in astrocytes leads to cell death, but the mechanism was unclear. This study shows JCV causes necrotic cell death, not apoptosis, in these glial cells.
Area of Science:
- Neurovirology
- Cell Biology
- Pathology
Background:
- John Cunningham virus (JCV) is a human neurotropic polyomavirus known to infect glial cells.
- JCV infection leads to lytic cell death, but the specific mechanism (apoptosis vs. necrosis) in astrocytes is not well understood.
Purpose of the Study:
- To investigate the mechanism of cell death induced by JCV infection in human central nervous system progenitor-derived astrocytes.
- To determine whether JCV-infected astrocytes undergo apoptosis or necrosis.
Main Methods:
- Utilized a human central nervous system progenitor-derived astrocyte cell culture model.
- Employed in situ DNA hybridization, immunocytochemistry, electron microscopy, and RNase protection assays.
- Assessed mRNA expression of caspase family genes and evaluated ultrastructural features of apoptosis.
Main Results:
- Astrocytes supported progressive JCV infection.
- Infected astrocytes exhibited features of necrotic cell death, including cytoplasmic vacuolization and organelle dissolution.
- No evidence of apoptosis was found, with no changes in caspase gene expression or detection of apoptotic markers.
Conclusions:
- JCV-induced cell death in progenitor cell-derived astrocytes occurs via necrosis, not apoptosis.
- The findings clarify the pathway of virus-induced cell death in this specific glial cell type.
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