ArticlePLoS pathogens2022
Inhibition of vaccinia virus L1 N-myristoylation by the host N-myristoyltransferase inhibitor IMP-1088 generates non-infectious virions defective in cell entry.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Infection cycles of viruses of the phylum Nucleocytoviricota.Nature reviews. Microbiology · 2026Review
- Inhibition of host N-myristoylation compromises the infectivity of SARS-CoV-2 due to Golgi-bypassing egress.Nature communications · 2026Article
- Drug repurposing against viral infections (2020-2025): clinical trials, computational strategies, and therapeutic interventions.Inflammopharmacology · 2026Review
- Vaccinia virus for lung cancer therapy: preclinical progress and prospects as a systemic immunotherapy platform.Frontiers in immunology · 2026Review
- Lumpy Skin Disease Virus Pathogenesis: Viral Protein Functions and Comparative Insights from Vaccinia Virus.Animals : an open access journal from MDPI · 2025Review
- Mechanism of cotranslational protein N-myristoylation in human cells.Molecular cell · 2025Article
- Article
- Repurposing Drugs for Synergistic Combination Therapies to Counteract Monkeypox Virus Tecovirimat Resistance.Viruses · 2025Article
- Structure of Plasmodium vivaxN-myristoyltransferase with inhibitor IMP-1088: exploring an NMT inhibitor for antimalarial therapy.Acta crystallographica. Section F, Structural biology communications · 2025Article
- Targeting n-myristoyltransferases promotes a pan-Mammarenavirus inhibition through the degradation of the Z matrix protein.PLoS pathogens · 2024Article
- HIV-1 N-myristoylation-dependent hijacking of late endosomes/lysosomes to drive Gag assembly in macrophages.Journal of cell science · 2024Article
- Protein lipidation in health and disease: molecular basis, physiological function and pathological implication.Signal transduction and targeted therapy · 2024Review
- Maturation of Viruses.Sub-cellular biochemistry · 2024Review
- Neutralization Determinants on Poxviruses.Viruses · 2023Review
- COPIng with senescence.Nature cell biology · 2023Article
- COPI vesicle formation and N-myristoylation are targetable vulnerabilities of senescent cells.Nature cell biology · 2023Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
We have recently shown that the replication of rhinovirus, poliovirus and foot-and-mouth disease virus requires the co-translational N-myristoylation of viral proteins by human host cell N-myristoyltransferases (NMTs), and is inhibited by treatment with IMP-1088, an ultrapotent small molecule NMT inhibitor. Here, we examine the importance of N-myristoylation during vaccinia virus (VACV) infection in primate cells and demonstrate the anti-poxviral effects of IMP-1088. N-myristoylated proteins from VACV and the host were metabolically labelled with myristic acid alkyne during infection using quantitative chemical proteomics. We identified VACV proteins A16, G9 and L1 to be N-myristoylated. Treatment with NMT inhibitor IMP-1088 potently abrogated VACV infection, while VACV gene expression, DNA replication, morphogenesis and EV formation remained unaffected. Importantly, we observed that loss of N-myristoylation resulted in greatly reduced infectivity of assembled mature virus particles, characterized by significantly reduced host cell entry and a decline in membrane fusion activity of progeny virus. While the N-myristoylation of VACV entry proteins L1, A16 and G9 was inhibited by IMP-1088, mutational and genetic studies demonstrated that the N-myristoylation of L1 was the most critical for VACV entry. Given the significant genetic identity between VACV, monkeypox virus and variola virus L1 homologs, our data provides a basis for further investigating the role of N-myristoylation in poxviral infections as well as the potential of selective NMT inhibitors like IMP-1088 as broad-spectrum poxvirus inhibitors.
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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 OpenQuestion graph.