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m5C RNA Methylation Is Dysregulated by Oncogenic Herpesviruses via c-Myc Signaling to Counteract Host Antiviral

Zhenyu Wu1, Dawei Zhou1, Zhixian He2

  • 1Department of Pathology, College of Medicine, The Ohio State University, Columbus, OH 43210, USA.

Biorxiv : the Preprint Server for Biology
|July 14, 2025
PubMed

Insights

Human gamma-herpesviruses like KSHV manipulate host RNA methylation to suppress antiviral defenses. This strategy aids viral replication by downregulating key factors such as TRIM25.

Area of Science:

  • Virology
  • Molecular Biology
  • Epigenetics

Background:

  • Herpesviruses employ immune evasion strategies for replication.
  • Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic gamma-herpesvirus.
  • Host immune suppression is overcome by KSHV through various mechanisms.

Purpose of the Study:

  • To investigate how KSHV dysregulates host 5-methylcytosine (m5C) modification and mRNA stability.
  • To identify viral strategies for overcoming host antiviral responses.
  • To understand the role of m5C RNA methylation in gamma-herpesvirus replication.

Main Methods:

  • RNA bisulfite sequencing (RNA-BS-seq) to identify m5C modifications.
  • Analysis of m5C RNA methyltransferases NSUN2 and NSUN1.
  • Investigating the impact of TRIM25 on KSHV replication.

Main Results:

  • KSHV infection downregulates m5C RNA methyltransferases NSUN2/1 via c-Myc suppression.
  • KSHV reduces m5C methylation and stability of TRIM25, a RIG-I pathway activator.
  • Depletion of NSUN2/1 or TRIM25 enhances KSHV lytic replication.
  • Similar mechanisms were observed with Epstein-Barr virus (EBV).

Conclusions:

  • Human gamma-herpesviruses utilize host m5C RNA methylation to suppress antiviral factors.
  • This manipulation promotes KSHV and EBV lytic replication.
  • Targeting m5C RNA methylation represents a novel viral immune evasion strategy.
Keywords:
KSHVNSUN1NSUN2RNA modificationTRIM25c-Myclatencylytic replicationreactivation

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