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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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Herpes Simplex Virus Organizes Cytoplasmic Membranes To Form a Viral Assembly Center in Neuronal Cells
Shaowen White1, Hiroyuki Kawano2, N Charles Harata2
1Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.
Journal of Virology
|July 24, 2020
Summary
Herpes simplex virus (HSV) forms a distinct cytoplasmic viral assembly center (cVAC) in neuronal cells, concentrating viral proteins and host membranes for efficient virus production. This organized factory is crucial for herpesvirus assembly and offers new therapeutic targets.
Area of Science:
- Virology
- Cell Biology
- Neuroscience
Background:
- Herpes simplex virus (HSV) is a neuroinvasive virus studied for herpesvirus properties.
- HSV assembly in epithelial cells is complex due to dispersed compartments.
- Understanding HSV assembly is key to controlling herpesvirus infections.
Purpose of the Study:
- To investigate the site of HSV assembly in neuronal cells.
- To identify viral and host factors involved in HSV assembly.
- To establish a model for studying common and cell-specific herpesvirus assembly.
Main Methods:
- Confocal microscopy to visualize viral assembly centers.
- Analysis of viral protein localization and host membrane association.
- Investigating the role of microtubules and viral protein pUL51 in cVAC formation.
Main Results:
- HSV forms a distinct, unitary cytoplasmic viral assembly center (cVAC) in neuronal cells.
- The cVAC concentrates viral structural proteins and is a major site of capsid envelopment.
- cVAC formation depends on microtubules and the viral protein pUL51, and concentrates Golgi and endosome-derived membranes.
Conclusions:
- The neuronal cVAC is a key site for HSV assembly and capsid envelopment.
- HSV cVAC formation provides a valuable model for studying herpesvirus assembly pathways.
- The cVAC highlights the importance of host membrane reorganization in viral replication.
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