ArticleEmerging microbes & infections2025
SARS-CoV-2 and HCoV-OC43 regulate host m6A modification via activation of the mTORC1 signalling pathway to facilitate viral replication.
Article in Emerging microbes & infections, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- N6-methyladenosine modification in the context of viral infection: from molecular mechanism to therapeutic potential.Virus research · 2026Review
- SARS-CoV-2 N Protein Hijacks the mViruses · 2026Article
- Viral-host interactions mediated by the mTOR signaling pathway.Cell insight · 2026Review
- Nanopore direct RNA sequencing reveals transmissible gastroenteritis virus epitranscriptomic and transcriptomic landscapes modulated by gene 7.Microbial genomics · 2026Article
- Astragalosides Promote MH7A Cell Apoptosis by Suppressing WTAP-mediated m6A Methylation of TRAIL-DR4.Combinatorial chemistry & high throughput screening · 2026Article
- N6-methyladenosine as a potential epitranscriptomic immune rheostat during SARS-CoV-2 infection.Frontiers in immunology · 2026Review
- Direct RNA sequencing reveals m6A modifications and isoform changes in SARS-CoV-2-infected HEK cells.Access microbiology · 2025Article
- Role of N6-Methyladenosine (m6A) epitranscriptomic mark in regulating viral infections and target for antiviral development.Frontiers in pharmacology · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-methyladenosine (m6A) is the most prevalent post-transcriptional modification in eukaryotic RNA and is also present in various viral RNAs, where it plays a crucial role in regulating the viral life cycle. However, the molecular mechanisms through which viruses regulate host RNA m6A methylation are not fully understood. In this study, we reveal that SARS-CoV-2 and HCoV-OC43 infection enhance host m6A modification by activating the mTORC1 signalling pathway. Specifically, the viral non-structural protein nsp14 upregulates the expression of S-adenosylmethionine synthase MAT2A in an mTORC1-dependent manner. This mTORC1-MAT2A axis subsequently stimulates the synthesis of S-adenosylmethionine (SAM). The increase of SAM then enhances the m6A methylation of host RNA and facilitates viral replication. Our findings uncover a molecular mechanism by which viruses regulate host m6A methylation and provide insights into how SARS-CoV-2 hijacks host cellular epitranscriptomic modifications to promote its replication.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.