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Updated: Nov 15, 2025

Porcine Corneal Tissue Explant to Study the Efficacy of Herpes Simplex Virus-1 Antivirals

Porcine Corneal Tissue Explant to Study the Efficacy of Herpes Simplex Virus-1 Antivirals

Published on: September 20, 2021

APOBECs and Herpesviruses.

Adam Z Cheng^1,2,3,4, Sofia N Moraes^1,2,3,4, Nadine M Shaban^1,2,3,4

¹Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.

|March 6, 2021

Summary

This summary is machine-generated.

Herpesviruses like EBV, KSHV, and HSV-1 evade APOBEC enzymes by using their ribonucleotide reductase (RNR) to bind and inhibit these antiviral proteins. This interaction protects viral DNA during replication and transmission.

Keywords:

APOBEC DNA cytosine deamination DNA editing evolution herpesvirus innate antiviral immunity mutation restriction factors ribonucleotide reductase

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Area of Science:

Virology
Immunology
Molecular Biology

Background:

APOBEC enzymes are crucial for innate immunity against viruses by deaminating cytosine in viral DNA.
Retroviruses like HIV-1 are well-established APOBEC targets, but evidence for herpesviruses was less clear.
Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), and herpes simplex virus-1 (HSV-1) are now recognized as potential APOBEC substrates.

Purpose of the Study:

To investigate the mechanisms by which herpesviruses evade APOBEC-mediated antiviral defense.
To elucidate the role of viral ribonucleotide reductase (RNR) in interacting with APOBEC enzymes.

Main Methods:

Investigated the interaction between herpesvirus RNR subunits and APOBEC3A/3B enzymes.
Utilized genetic inactivation of EBV RNR (BORF2) to assess its impact on viral infectivity and mutation rates.
Analyzed APOBEC-mediated C-to-U deamination and G-to-A hypermutation in viral DNA.

Main Results:

Herpesviruses, including EBV, KSHV, and HSV-1, have evolved to repurpose their RNR large subunits to bind and inhibit APOBEC3A and APOBEC3B.
Genetic inactivation of EBV RNR (BORF2) led to reduced viral infectivity and increased C/G-to-T/A hypermutation.
The RNR-APOBEC interaction is critical for protecting viral DNA replication intermediates during the lytic phase.

Conclusions:

Herpesviruses engage in a novel host-pathogen conflict involving RNR-mediated inhibition of APOBEC enzymes.
This RNR-APOBEC interaction is essential for successful viral transmission and pathogenesis.
While crucial for immediate defense, partial loss of RNR-APOBEC interaction may provide mutational flexibility for viral adaptation over evolutionary timescales.