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Morphogenesis of measles virus on C6 rat glioma cells
K Röser1, W Bohn, K Mannweiler
1Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie, Universität Hamburg, F.R.G.
Journal of Neuroimmunology
|December 1, 1988
Abstract:
Rat glioma cells (C6) persistently infected with measles virus show a locally dissociated distribution of budding processes at the cell surface.
Insights
Measles virus infection in rat glioma cells causes abnormal budding processes. This disruption affects cell surface organization in persistently infected C6 cells.
Area of Science:
- Cell Biology
- Virology
- Neuro-oncology
Background:
- Persistent viral infections can alter cellular functions and morphology.
- Measles virus (MeV) is a paramyxovirus with implications for various cell types, including neural cells.
Purpose of the Study:
- To investigate the impact of persistent measles virus infection on the ultrastructure of rat glioma cells (C6).
- To characterize the distribution of viral budding processes on the surface of infected glioma cells.
Main Methods:
- Culturing of rat glioma C6 cells.
- Establishment of persistent measles virus infection in C6 cells.
- Electron microscopy to visualize cell surface and budding structures.
Main Results:
- Rat glioma C6 cells persistently infected with measles virus exhibited a disorganized pattern of viral budding.
- Budding processes were not uniformly distributed but showed localized dissociation at the cell surface.
- Alterations in cell surface morphology were observed in conjunction with viral budding.
Conclusions:
- Persistent measles virus infection disrupts the normal organization of viral budding in rat glioma cells.
- The findings suggest that measles virus can induce significant changes in the cellular architecture of glioma cells.
- Further research is warranted to understand the mechanisms behind this dissociation and its functional consequences.