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Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules
Published on: May 12, 2017
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Infectious Bronchitis Virus Regulates Cellular Stress Granule Signaling
Matthew J Brownsword1,2, Nicole Doyle1, Michèle Brocard2
1The Pirbright Institute, Pirbright, Surrey GU24 0NF, UK.
Viruses
|May 20, 2020
Summary
The infectious bronchitis virus (IBV) inhibits cellular stress responses that normally block viral gene expression. IBV also induces stress granules independently of translation inhibition, offering new insights into viral evasion strategies.
Area of Science:
- Molecular Biology
- Virology
- Cell Biology
Background:
- Viruses rely on host cell translation for gene expression.
- Cellular stress responses globally inhibit translation and form stress granules, silencing most mRNAs.
- Some stress responses maintain expression of antiviral factors during infection.
Purpose of the Study:
- To investigate how the Gammacoronavirus infectious bronchitis virus (IBV) regulates cellular stress granules.
- To understand IBV's modulation of cellular translation and antiviral signaling during infection.
Main Methods:
- Investigated stress granule formation and regulation during IBV infection.
- Analyzed the impact of IBV on cellular stress granule signaling pathways.
- Assessed the relationship between translational repression, stress granule formation, and eIF2α phosphorylation.
Main Results:
- IBV inhibits multiple cellular stress granule signaling pathways.
- IBV replication induces stress granules in a subset of infected cells.
- IBV infection uncouples translational repression from stress granule formation, independent of eIF2α phosphorylation.
Conclusions:
- IBV actively modulates host cell translation and stress responses.
- IBV employs distinct mechanisms to overcome cellular antiviral defenses.
- Findings provide novel insights into viral strategies for replication amidst host stress.
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