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08:26
Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins
Published on: August 31, 2017
Chromatin dynamics during lytic infection with herpes simplex virus 1
Kristen L Conn1, Luis M Schang
1Department of Biochemistry, Li Ka Shing Institute of Virology, University of Alberta, Edmonton, AB T6G 2H7, Canada. kconn@ualberta.ca
Viruses
|July 19, 2013
Summary
Herpes Simplex Virus type 1 (HSV-1) genomes in infected cells are dynamic, reconciling low histone occupancy with chromatin modifications that regulate viral gene expression.
Area of Science:
- Virology
- Epigenetics
- Molecular Biology
Background:
- Latent HSV-1 genomes are chromatinized with silencing marks.
- Studies since 2004 showed inconsistencies regarding HSV-1 genome chromatinization during lytic infection.
- Nuclease protection and ChIP assays indicated low histone occupancy, suggesting irregular chromatinization.
Purpose of the Study:
- To reconcile conflicting findings on HSV-1 genome chromatinization during lytic infection.
- To investigate the role of chromatin modifications and remodeling in HSV-1 gene regulation.
- To understand the dynamic interplay between viral and cellular chromatin.
Main Methods:
- Nuclease protection assays
- Chromatin immunoprecipitation (ChIP) assays
- Analysis of chromatin modifications on viral genes
- Investigating interactions between HSV-1 transcriptional activators and chromatin-modifying enzymes
- Depletion and overexpression of chromatin-modifying proteins
Main Results:
- Chromatin modifications on HSV-1 genes correlated with active or repressed transcription.
- HSV-1 transcriptional activators can induce chromatin remodeling and interact with modifying enzymes.
- Modulation of chromatin modifiers affected HSV-1 transcription, sometimes unexpectedly.
- Since 2010, evidence points to dynamic cellular and HSV-1 chromatin in infected cells.
Conclusions:
- Viral and cellular chromatin dynamics in infected cells explain the apparent inconsistencies in HSV-1 genome chromatinization.
- These dynamics reconcile low histone occupancy with chromatin-based regulation of HSV-1 gene expression.
- The dynamic nature of chromatin explains unexpected outcomes when modulating chromatin remodeling activities.
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