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Related Experiment Video

Updated: May 17, 2026

Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy

Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy

Published on: November 4, 2018

Efficient herpes simplex virus 1 replication requires cellular ATR pathway proteins.

Kareem N Mohni¹, Alexander R Dee, Samantha Smith

¹Department of Molecular, Microbial and Structural Biology and the Molecular Biology and Biochemistry Graduate Program, University of Connecticut Health Center, Farmington, Connecticut, USA.

Journal of Virology

|October 26, 2012

Summary

Herpes simplex virus 1 (HSV-1) proteins are recruited to replication sites. While essential for HSV-1 replication, activating the ATR pathway inhibits viral recombination.

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Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy

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Area of Science:

Virology
Molecular Biology
Cellular Biology

Background:

Herpes simplex virus 1 (HSV-1) interacts with host DNA damage response (DDR) machinery.
ATR kinase is inactivated in HSV-1-infected cells, yet ATR and ATRIP aid viral replication.

Purpose of the Study:

Investigate the dual role of ATR pathway proteins in HSV-1 infection.
Determine if ATR pathway components have antiviral effects.

Main Methods:

Assessed stability and localization of ATR pathway proteins in HSV-infected cells.
Utilized short hairpin RNA (shRNA) for gene knockdown.
Measured viral yield and inter-viral recombination after ATR kinase activation.

Main Results:

All 10 canonical ATR pathway proteins are stable and recruited to viral replication compartments.
Knockdown of ATRIP, RPA70, TopBP1, Claspin, and CINP impairs HSV-1 replication.
ATR kinase activation pre-infection did not alter virus yield but reduced viral recombination.

Conclusions:

ATR pathway proteins are not inherently antiviral but are crucial for efficient HSV-1 replication.
ATR pathway activation may negatively impact viral replication by inhibiting recombination.