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Related Experiment Video

Updated: Apr 12, 2026

Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins

Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins

Published on: August 31, 2017

Upstream binding factor inhibits herpes simplex virus replication.

Gabriel Ouellet Lavallée¹, Angela Pearson¹

¹INRS-Institut Armand-Frappier, Laval, Québec, Canada.

|May 13, 2015

Summary

This summary is machine-generated.

Upstream Binding Factor (UBF) normally relocates during herpes simplex virus (HSV) infection. Surprisingly, depleting UBF enhances HSV replication and gene expression, suggesting UBF restricts viral DNA activity before replication.

Keywords:

Herpes simplex virus Intrinsic antiviral response Upstream Binding Factor Viral DNA replication Viral transcription

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Area of Science:

Virology
Molecular Biology
Cell Biology

Background:

Herpes simplex virus 1 (HSV-1) infection alters the host cell nucleus.
Cellular protein Upstream Binding Factor (UBF) relocalizes from the nucleolus to viral replication compartments (VRCs) during HSV-1 infection.

Purpose of the Study:

To investigate the role of UBF in HSV replication.
To test the hypothesis that UBF is recruited to VRCs to promote viral DNA replication.

Main Methods:

Depletion of UBF in HeLa cells and human foreskin fibroblasts.
Infection with HSV-1 and HSV-2.
Quantification of viral titers, viral DNA, and viral gene expression (mRNA and protein).

Main Results:

UBF depletion resulted in significantly higher viral titers for both HSV-1 and HSV-2.
Reduced UBF expression led to increased HSV-1 DNA levels and elevated expression of HSV-1 ICP27 and TK.
These effects were observed irrespective of viral DNA replication inhibition.

Conclusions:

UBF appears to inhibit gene expression from viral DNA prior to replication.
This study is the first to report a restrictive role for UBF in viral replication.
UBF's function in HSV infection is contrary to the initial hypothesis, revealing a novel inhibitory mechanism.