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Updated: Jul 22, 2026

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.
Abstract:
Plaque area is a measure of the degree of cytopathic effect and a predictor of neurovirulence for tissue culture adapted morbilliviruses. In the present work, the cellular stress response was shown to be a determinant of the expression of distinct measles virus large plaque phenotypes in Vero cells. The emergence of these large plaque phenotypes was associated with increased mean viral transcriptional activity and expression of the viral fusion glycoprotein, but not upregulation of the virus receptor CD46.
Insights
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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