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Related Experiment Video

Updated: Apr 16, 2026

Targeted in Situ Mutagenesis of Histone Genes in Budding Yeast

Targeted in Situ Mutagenesis of Histone Genes in Budding Yeast

Published on: January 26, 2017

Herpes simplex virus type 1 R-loops are targets for APOBEC-mediated mutagenesis.

Márton Miskei^1,2,3, Dóra Varga^1,4, Lilla Hornyák¹

¹MTA-DE Momentum Genome Architecture and Recombination Research Group, Department of Molecular and Nanopharmaceutics, Faculty of Pharmacy, University of Debrecen, Debrecen, Hungary.

|April 14, 2026

Summary

This summary is machine-generated.

APOBEC3 enzymes target viral R-loops, causing mutations essential for antiviral immunity during herpes simplex virus type 1 infections. This R-loop and APOBEC3 interaction reveals a key vulnerability in viral replication.

Keywords:

APOBEC DRIP-seq HSV-1 R-loop RNA–DNA hybrid Virus

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Published on: July 12, 2013

Area of Science:

Molecular Biology
Virology
Immunology

Background:

APOBEC3 enzymes are crucial for innate antiviral immunity.
These enzymes function by introducing mutations into viral DNA.
Herpes simplex virus type 1 (HSV-1) is a common human pathogen.

Purpose of the Study:

To investigate the role of R-loops in APOBEC3-mediated mutagenesis during HSV-1 infection.
To identify the specific substrates and mechanisms of APOBEC3 activity against HSV-1.

Main Methods:

Utilized molecular biology techniques to study R-loop formation in HSV-1 infected cells.
Investigated the recruitment and activity of APOBEC3 enzymes in the presence of viral R-loops.
Analyzed mutation patterns in viral genomes to assess APOBEC3-mediated mutagenesis.

Main Results:

Viral R-loops were identified as preferred substrates for APOBEC3 enzymes during HSV-1 infection.
APOBEC3 enzymes were recruited to these viral R-loops.
Mutagenesis occurred specifically upon the interaction of R-loops and APOBEC3 enzymes, leading to clustered C-to-T mutations in viral genes.
R-loops alone were not mutagenic, and APOBEC3 enzymes did not edit HSV-1 in the absence of R-loops.

Conclusions:

Endogenous R-loops formed during HSV-1 infection represent critical vulnerabilities.
The coupling of R-loops and APOBEC3 enzymes is a significant mechanism for antiviral mutagenesis.
Targeting R-loop formation or APOBEC3 activity could be potential antiviral strategies.