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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
The cellular stress response increases measles virus-induced cytopathic effect
D Vasconcelos1, E Norrby, M Oglesbee
1Department of Veterinary Biosciences, The Ohio State University, Columbus 43210-1093, USA.
The Journal of General Virology
|July 29, 1998
Summary
Cellular stress response influences measles virus plaque size in Vero cells. This affects viral transcription and fusion glycoprotein expression, impacting neurovirulence prediction.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Plaque area quantifies cytopathic effect and predicts morbillivirus neurovirulence in cell culture.
- Measles virus (MeV) exhibits distinct plaque phenotypes, with large plaques potentially indicating altered virulence.
Purpose of the Study:
- To investigate the role of cellular stress response in the development of distinct measles virus large plaque phenotypes.
- To determine the association between large plaque phenotypes and viral gene expression or receptor utilization.
Main Methods:
- Utilized Vero cells to culture measles virus and induce distinct plaque phenotypes.
- Analyzed viral transcriptional activity and expression of the viral fusion glycoprotein.
- Assessed the expression of the virus receptor CD46 in relation to plaque size.
Main Results:
- Cellular stress response was identified as a key determinant for expressing distinct measles virus large plaque phenotypes.
- Emergence of large plaque phenotypes correlated with increased mean viral transcriptional activity.
- Increased expression of the viral fusion glycoprotein was observed in large plaque phenotypes.
- No significant upregulation of the virus receptor CD46 was detected in association with large plaques.
Conclusions:
- Cellular stress significantly impacts measles virus plaque morphology and gene expression.
- The cellular stress response is a critical factor in modulating measles virus virulence phenotypes.
- Understanding these mechanisms may refine neurovirulence prediction for morbilliviruses.
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