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Updated: Jun 3, 2026
08:26
Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins
Published on: August 31, 2017
Analysis of HSV Polypeptides
1National Centre for Research in Virology, University of Bergen, Bergen High Technology Centre, Bergen, Norway.
Methods in Molecular Medicine
|March 5, 2011
Summary
Herpes simplex virus (HSV) infection shuts down most cellular protein production but allows some viral proteins to be made. Certain cellular genes are activated during HSV infection, impacting virus replication.
Area of Science:
- Virology
- Molecular Biology
- Cellular Biology
Background:
- Herpes simplex virus (HSV) infection involves complex interactions between viral and host cellular machinery.
- HSV efficiently inhibits host cell protein synthesis during lytic infection.
- Specific viral proteins, like V(MW)65 and IE 110, interact with host factors.
Purpose of the Study:
- To investigate the intricate mechanisms of host protein synthesis inhibition by HSV.
- To identify cellular proteins and genes that are either suppressed or activated during HSV infection.
- To understand the role of specific viral regulatory proteins in modulating host cell responses.
Main Methods:
- Analysis of protein synthesis profiles in HSV-infected cells.
- Identification of viral proteins involved in host shutoff.
- Investigation of host gene expression changes post-infection.
Main Results:
- HSV infection effectively suppresses the synthesis of most host cellular proteins.
- A subset of viral proteins, including host shutoff factors, are produced during infection.
- Some host proteins interacting with viral regulatory proteins (V(MW)65, IE 110) are still synthesized.
- Specific quiescent cellular genes are activated following HSV infection.
Conclusions:
- HSV employs sophisticated strategies to control host protein synthesis, favoring viral replication.
- The interplay between viral regulatory proteins and host factors is crucial for successful HSV infection.
- HSV infection induces a dynamic reprogramming of host gene expression, with both suppression and activation occurring.
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