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HSV-1 remodels host telomeres to facilitate viral replication
Zhong Deng1, Eui Tae Kim2, Olga Vladimirova1
1The Wistar Institute, Philadelphia, PA 19104, USA.
Cell Reports
|December 16, 2014
Summary
Herpes simplex virus 1 (HSV-1) infection causes telomere damage and dysfunction. The virus degrades a key telomere protein, TPP1, to promote its own replication, suggesting telomeres are reorganized for viral DNA synthesis.
Area of Science:
- Molecular Biology
- Virology
- Genetics
Background:
- Telomeres are crucial protective caps at the ends of chromosomes.
- Telomere dysfunction can lead to genomic instability and disease.
- Herpes simplex virus 1 (HSV-1) is a common human pathogen.
Purpose of the Study:
- To investigate the effects of HSV-1 infection on telomeres.
- To elucidate the molecular mechanisms by which HSV-1 interacts with telomeres.
- To understand the role of telomere-associated proteins in HSV-1 replication.
Main Methods:
- Analysis of chromosomal aberrations in HSV-1 infected cells.
- Measurement of telomere repeat-containing RNA (TERRA) transcription.
- Assessment of telomere protein TPP1 degradation.
- Viral replication assays using shRNA and ICP8-null virus.
Main Results:
- HSV-1 infection induced telomere structural aberrations and DNA damage foci (TIFs).
- HSV-1 promoted TERRA transcription and TPP1 degradation, mediated by the viral ICP0 protein.
- Depletion of TPP1 enhanced viral replication, indicating an inhibitory role for TPP1.
- Viral protein ICP8 localized to telomeres and was essential for telomere DNA signal degradation.
Conclusions:
- HSV-1 infection actively reorganizes telomeres, creating ICP8-associated prereplication sites.
- This telomere reorganization facilitates HSV-1 genomic replication.
- Telomere-associated proteins play a significant role in regulating HSV-1 replication.
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