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Updated: Jul 20, 2025

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Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy
Published on: November 4, 2018
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HSV-1 exploits host heterochromatin for nuclear egress
Hannah C Lewis1,2, Laurel E Kelnhofer-Millevolte1,2,3, Mia R Brinkley1
1Human Biology Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
The Journal of Cell Biology
|July 30, 2023
Summary
Herpes simplex virus (HSV-1) uses host heterochromatin, including H3K27me3 and macroH2A1, for efficient nuclear egress. Loss of these marks traps viral capsids, reducing viral spread.
Area of Science:
- Virology
- Epigenetics
- Cell Biology
Background:
- Herpes simplex virus type 1 (HSV-1) replication involves progeny capsid formation and egress from the host cell nucleus.
- Efficient viral egress requires navigating the complex nuclear chromatin environment.
Purpose of the Study:
- To investigate the role of host heterochromatin, specifically H3K27me3 and macroH2A1, in HSV-1 capsid nuclear egress.
- To understand how HSV-1 interacts with and potentially manipulates host chromatin during infection.
Main Methods:
- Transmission electron microscopy (TEM) to visualize HSV-1 capsids within the nucleus.
- Chromatin profiling to analyze the distribution of H3K27me3 and macroH2A1 during HSV-1 infection.
- Live-capsid tracking to quantify capsid movement within the nucleus.
Main Results:
- HSV-1 capsids were observed traversing heterochromatin marked by H3K27me3 and macroH2A1.
- Infection led to global redistribution of H3K27me3 and macroH2A1, correlating with decreased host transcription.
- Loss of H3K27me3 or macroH2A1 significantly reduced viral titers and caused nuclear trapping of capsids, impairing egress.
Conclusions:
- HSV-1 utilizes host heterochromatin dynamics, including H3K27me3 and macroH2A1, to facilitate efficient nuclear egress.
- These epigenetic modifications are crucial for viral capsid movement and successful exit from the nucleus.
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