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<p>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.</p>

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月14日

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  • Márton Miskei,
  • Dóra Varga,
  • Lilla Hornyák,
  • Éva Sipos,
  • Éva Nagy,
  • Qiuzhen Li,
  • Zsolt Karányi,
  • Zoltán Szabó,
  • Rachel DeWeerd,
  • Abby M. Green,
  • Dávid Szüts,
  • Eszter Csoma,
  • Lóránt Székvölgyi

摘要

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.