ArticlePLoS pathogens2024
Classical swine fever virus non-structural protein 5B hijacks host METTL14-mediated m6A modification to counteract host antiviral immune response.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 8 citations in OpenAlex.
- Oral Food-Derived Proanthocyanidins as Immunostimulants: Enhanced Vaccine Immunogenicity via Host Immune Modulation in a Murine CSFV Model.Molecules (Basel, Switzerland) · 2026Article
- N6-methyladenosine modification in the context of viral infection: from molecular mechanism to therapeutic potential.Virus research · 2026Review
- YTHDF2 in inflammation: Mechanisms and therapeutic strategies.Genes & diseases · 2026Review
- METTL14-Mediated Inhibition of Apoptosis via the MAPK and PI3K/AKT Pathways PromotesMicroorganisms · 2026Article
- Review
- Landscape of NFrontiers in microbiology · 2026Article
- SUMOylation-dependent degradation of nucleocapsid is responsible forJournal of virology · 2025Article
- Flaviviridae RdRp exploits NSUN2-driven m5C methylation to establish persistent infection.PLoS pathogens · 2025Article
- The m6A demethylase FTO regulates TNF-α expression in human macrophages following Toxoplasma gondii infection.PLoS neglected tropical diseases · 2025Article
- Role of N6-Methyladenosine (m6A) epitranscriptomic mark in regulating viral infections and target for antiviral development.Frontiers in pharmacology · 2025Review
- When animal viruses meet NVeterinary research · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Classical Swine Fever (CSF), caused by the Classical Swine Fever Virus (CSFV), inflicts significant economic losses on the global pig industry. A key factor in the challenge of eradicating this virus is its ability to evade the host's innate immune response, leading to persistent infections. In our study, we elucidate the molecular mechanism through which CSFV exploits m6A modifications to circumvent host immune surveillance, thus facilitating its proliferation. We initially discovered that m6A modifications were elevated both in vivo and in vitro upon CSFV infection, particularly noting an increase in the expression of the methyltransferase METTL14. CSFV non-structural protein 5B was found to hijack HRD1, the E3 ubiquitin ligase for METTL14, preventing METTL14 degradation. MeRIP-seq analysis further revealed that METTL14 specifically targeted and methylated TLRs, notably TLR4. METTL14-mediated regulation of TLR4 degradation, facilitated by YTHDF2, led to the accelerated mRNA decay of TLR4. Consequently, TLR4-mediated NF-κB signaling, a crucial component of the innate immune response, is suppressed by CSFV. Collectively, these data effectively highlight the viral evasion tactics, shedding light on potential antiviral strategies targeting METTL14 to curb CSFV infection.
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Registered trials
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 OpenQuestion graph.