ArticleGenes & diseases2022
Targeting m6A modification inhibits herpes virus 1 infection.
Article in Genes & diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- N6-methyladenosine modification in the context of viral infection: from molecular mechanism to therapeutic potential.Virus research · 2026Review
- Neuromodulatory role and therapeutic potential of N 6 -methyladenosine RNA methylation in neurodegenerative diseases.Neural regeneration research · 2026Article
- WTAP stabilized by USP7 contributes to enzalutamide resistance in prostate cancer via mediating AKT mCancer gene therapy · 2026Article
- N6-methyladenosine within transmissible gastroenteritis virus genomic RNA inhibits its replication via efficient recognition by RNA sensor RIG-I.Journal of virology · 2026Article
- Carbon Quantum Dots Assisted Virus Tracking: From Skin to Brain.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- CAPRIN1 specifically mediates mCommunications biology · 2025Article
- N6-methyladenosine modification of HCMV IE1 transcript promotes the repressive state of viral genome to achieve latent infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Strain-Divergent m6A Landscapes Modulate Nipah Virus Replication and METTL3 Inhibition Attenuates Virulence.Viruses · 2025Article
- Herpesviruses: overview of systematics, genomic complexity and life cycle.Virology journal · 2025Review
- Correlation of METTL4 genetic variants and severe pneumonia pediatric patients in Southern China.BMC genomic data · 2025Article
- The role of NJournal of virology · 2025Review
- The Tiny Epigenetic Addition Plays Big Roles: The RNA Methylation in Both Human and Animal Herpesvirus Infection.Transboundary and emerging diseases · 2025Review
- Role of N6-Methyladenosine (m6A) epitranscriptomic mark in regulating viral infections and target for antiviral development.Frontiers in pharmacology · 2025Review
- Epigenetic regulation-mediated disorders in dopamine transporter endocytosis: A novel mechanism for the pathogenesis of Parkinson's disease.Theranostics · 2025Review
- Depletion of mMicrobiology spectrum · 2024Article
- RNA Modifications in Pathogenic Viruses: Existence, Mechanism, and Impacts.Microorganisms · 2024Review
- m6A demethylase FTO transcriptionally activated by SP1 improves ischemia reperfusion-triggered acute kidney injury by activating Ambra1/ULK1-mediated autophagy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Article
- Insights into RNA N6-methyladenosine and programmed cell death in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2024Review
- GnRH-driven FTO-mediated RNA mBMC biology · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The latent infection by herpes virus type 1 (HSV-1) may be lifelong in trigeminal ganglia and a suspected cause of Alzheimer's Disease (AD) and Amyotrophic lateral sclerosis (ALS). Whether and how N6-methyladenosine (m6A) modification of viral RNAs affects virus infection are poorly understood. Here, we report that HSV-1 infection enhanced the expression of m6A writers (METTL3, METTL14) and readers (YTHDF1/2/3) at the early infection stage and decreased their expression later on, while suppressed the erasers' (FTO, ALBKH5) expression immediately upon infection to facilitate viral replication. Inhibiting m6A modification by 3-deazaadenosine (DAA) significantly decreased viral replication and reduced viral reproduction over 1000 folds. More interestingly, depleting the writers and readers by siRNAs inhibited virus replication and reproduction; whereas depleting the erasers promoted viral replication and reproduction. Silencing YTHDF3 strikingly decreased viral replication by up to 90%, leading to reduction of up to 10-fold viral replication and over 100-fold virus reproduction, respectively. Depletion of m6A initiator METTL3 (by 60%-70%) by siRNA correlatedly decreased viral replication 60%-70%, and reduced virus yield over 30-fold. Consistently, ectopic expression of METTL3 largely increased virus yield. METTL3 knockdown suppressed the HSV-1 intermediate early and early genes (ICP0, ICP8 and UL23) and late genes (VP16, UL44, UL49 and ICP47); while ectopic expression of METTL3 upregulated these gene expression. Results from our study shed the lights on the importance for m6A modification to initiate HSV-1 early replication. The components of m6A modification machinery, particularly m6A initiator METTL3 and reader YTHDF3, would be potential important targets for combating HSV-1 infections.
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