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08:26
Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins
Published on: August 31, 2017
Nucleolin is required for an efficient herpes simplex virus type 1 infection.
Aleth Callé1, Iva Ugrinova, Alberto L Epstein
1Université de Lyon, Lyon F-69003, France.
Journal of Virology
|March 7, 2008
Summary
Herpes simplex virus type 1 (HSV-1) infection disrupts host cell nucleoli, causing nucleolin to relocate and aid viral DNA replication. High nucleolin levels are essential for effective viral replication, revealing its direct role in HSV-1 biology.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Herpes simplex virus type 1 (HSV-1) infection significantly alters host cell nuclear architecture, particularly nucleolar morphology.
- Key nucleolar proteins, including nucleolin, B23, and fibrillarin, are known to be affected during viral infections.
Purpose of the Study:
- To investigate the role of nucleolar proteins, specifically nucleolin, during productive HSV-1 infection.
- To determine the impact of HSV-1 infection on nucleolin localization and its involvement in viral replication.
Main Methods:
- Immunofluorescence microscopy to track nucleolin localization during HSV-1 infection.
- Western blotting to quantify nucleolin levels.
- Small interfering RNA (siRNA) technology to assess the effect of nucleolin depletion on viral replication.
- Analysis of viral protein ICP4 and ICP8 interactions.
Main Results:
- HSV-1 infection causes the redistribution of nucleolin, B23, and fibrillarin from nucleoli.
- Nucleolin levels increase during infection and colocalize with viral protein ICP8 in replication compartments, suggesting a role in HSV-1 DNA replication.
- A granular form of nucleolin accumulates in aggresomes, indicating degradation.
- Nucleolin delocalization depends on the viral ICP4 protein.
- Viral replication requires high nucleolin expression, confirmed by siRNA experiments.
Conclusions:
- Nucleolin plays a direct and essential role in herpes simplex virus biology, particularly in viral DNA replication.
- The modulation and utilization of nucleolin by HSV-1 highlight a novel interaction between viral and host cell machinery.
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