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Updated: May 22, 2026
09:33
Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules
Published on: May 12, 2017
Herpes simplex virus 2 infection impacts stress granule accumulation
Renée L Finnen1, Kyle R Pangka, Bruce W Banfield
1Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Journal of Virology
|May 25, 2012
Summary
Herpes simplex virus 2 (HSV-2) infection prevents stress granule (SG) formation, even when translation is inhibited. This suggests HSV-2 has unique mechanisms to maintain protein synthesis during infection.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Viral infections often disrupt host cell processes, including the formation of stress granules (SGs), which are involved in translational regulation.
- Understanding how viruses manipulate SG formation is crucial for comprehending viral replication strategies.
Purpose of the Study:
- To investigate the impact of herpes simplex virus 2 (HSV-2) infection on stress granule (SG) accumulation.
- To identify the mechanisms by which HSV-2 interferes with SG formation and translation.
Main Methods:
- Monitoring the localization of SG components (TIA-1, G3BP, PABP) in HSV-2 infected cells.
- Inducing SG formation using arsenite and pateamine A, with and without HSV-2 infection.
- Analyzing the role of eukaryotic translation initiation factor 2α (eIF2α) phosphorylation and viral DNA replication in SG dynamics.
Main Results:
- HSV-2 infection inhibited arsenite-induced SG accumulation, despite increased eIF2α phosphorylation.
- Pateamine A-induced SGs in infected cells lacked TIA-1 but contained G3BP and PABP.
- Novel TIA-1-containing nuclear structures, associated with Sam68, formed late in infection and depended on viral DNA replication.
Conclusions:
- HSV-2 possesses mechanisms to inhibit SG formation and maintain translation, independent of eIF2α phosphorylation.
- Distinct SG populations form under different induction conditions in HSV-2 infected cells.
- Late viral replication events lead to the formation of TIA-1/Sam68 nuclear structures.
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