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N6-methyladenosine (m6A) modification regulates LONP1 to inhibit coxsackievirus B3 replication by suppressing

Wang Qimeng1, Yan Wang1, Tingjun Liu2

  • 1Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, Department of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, 212013, PR China.

International Journal of Biological Macromolecules
|November 29, 2025
PubMed

Insights

This study reveals how N6-methyladenosine (m6A) RNA modification regulates mitochondrial protease LONP1 to combat Coxsackievirus B3 (CVB3) infection. Upregulating LONP1 inhibits viral replication and reduces ferroptosis, offering new therapeutic targets for enteroviral diseases.

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Coxsackievirus B3 (CVB3) causes myocarditis and pancreatitis with no effective treatments.
  • Understanding CVB3 pathogenesis is crucial for developing therapies.
  • N6-methyladenosine (m6A) RNA modification is increasingly recognized for its role in viral infections.

Purpose of the Study:

  • To investigate the role of m6A RNA modification in regulating mitochondrial protease LONP1 during CVB3 infection.
  • To elucidate the mechanism by which CVB3 affects LONP1 expression.
  • To determine the functional significance of LONP1 in CVB3 replication and host cell response.

Main Methods:

  • Methylated RNA immunoprecipitation (MeRIP) to assess m6A levels.
  • Dual-luciferase assays to confirm m6A modification sites.
  • Western blotting and viral titer assays to measure viral replication.
  • Analysis of ferroptosis markers (GPX4, ACSL4), intracellular iron, and ROS levels.

Main Results:

  • CVB3 infection reduced m6A levels on LONP1 mRNA, leading to increased LONP1 expression.
  • CVB3 protein 2B degraded WTAP, decreasing m6A deposition on LONP1 mRNA.
  • Reduced m6A stabilized LONP1 mRNA by impairing YTHDF2-mediated decay.
  • LONP1 overexpression inhibited CVB3 replication and mitigated ferroptosis.
  • LONP1 silencing exacerbated viral replication and ferroptotic damage.

Conclusions:

  • LONP1 acts as an m6A-regulated antiviral factor suppressing CVB3 replication.
  • LONP1 inhibits CVB3-induced ferroptosis by modulating key cellular pathways.
  • Targeting m6A machinery or LONP1 offers potential therapeutic strategies for enteroviral infections.
Keywords:
Coxsackievirus B3EnterovirusFerroptosisLONP1m(6)A

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