Published March 8, 2026
| Version v1
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Microscopic data for: Herpes simplex virus type 1 R-loops are targets for APOBEC-mediated mutagenesis
Authors/Creators
-
1.
University of Debrecen
- 2. Washington University School of Medicine, St. Louis, MO, United States
- 3. Research Centre for Natural Sciences
Description
APOBEC3 enzymes are key effectors of antiviral immunity that introduce mutations into viral genomes. We show that viral R-loops serve as preferred substrates for APOBEC3-mediated mutagenesis during herpes simplex virus type 1 (HSV-1) infection. APOBEC3 enzymes are recruited to viral R-loops, generating clustered C-to-T mutations in genes critical for viral assembly. Importantly, R-loops alone are not mutagenic, and APOBEC3 enzymes do not edit HSV-1 without an R-loop; mutagenesis occurs when R-loops and APOBEC3 enzymes interact. These findings identify endogenous R-loops formed during the HSV-1 life cycle as focal vulnerabilities and highlight R-loop–APOBEC3 coupling as a mechanism for antiviral mutagenesis.
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Figure 1B.zip
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