ArticleThe Journal of clinical investigation2018
Human tryptophanyl-tRNA synthetase is an IFN-γ-inducible entry factor for Enterovirus.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed.
- Plasma proteomics for biomarker discovery in childhood tuberculosis.Nature communications · 2025Article
- Editorial: Molecular pathogenesis of enteroviruses: insights into viral-host interactions, pathogenic mechanisms, and microbiome dynamics.Frontiers in microbiology · 2025Article
- Vascular endothelial growth factor receptor 2 as a potential host target for the inhibition of enterovirus replication.Journal of virology · 2024Article
- Transcriptomic Signatures of Zika Virus Infection in Patients and a Cell Culture Model.Microorganisms · 2024Article
- Pseudorabies virus manipulates mitochondrial tryptophanyl-tRNA synthetase 2 for viral replication.Virologica Sinica · 2024Article
- Zika virus infection in a cell culture model reflects the transcriptomic signatures in patients.bioRxiv : the preprint server for biology · 2024Article
- Enterovirus A71 does not meet the uncoating receptor SCARB2 at the cell surface.PLoS pathogens · 2024Article
- Aminoacyl-tRNA synthetase interactions in SARS-CoV-2 infection.Biochemical Society transactions · 2023Review
- A viral pan-end RNA element and host complex define a SARS-CoV-2 regulon.Nature communications · 2023Article
- Review
- Current status of hand-foot-and-mouth disease.Journal of biomedical science · 2023Review
- Vemurafenib Inhibits Enterovirus A71 Genome Replication and Virus Assembly.Pharmaceuticals (Basel, Switzerland) · 2022Article
- SLC35B2 Acts in a Dual Role in the Host Sulfation Required for EV71 Infection.Journal of virology · 2022Article
- Interferon-gamma inhibits influenza A virus cellular attachment by reducing sialic acid cluster size.iScience · 2022Article
- Enterovirus A71 antivirals: Past, present, and future.Acta pharmaceutica Sinica. B · 2022Article
- Review
- Molecular Docking of SP40 Peptide towards Cellular Receptors for Enterovirus 71 (EV-A71).Molecules (Basel, Switzerland) · 2021Article
- Molecular determinants and heterogeneity underlying host response to EV-A71 infection at single-cell resolution.RNA biology · 2021Article
- Article
- Human Intestinal Organoids Recapitulate Enteric Infections of Enterovirus and Coronavirus.Stem cell reports · 2021Article
Corrections and comments
- Commented on by
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus A71 (EV-A71) receptors that have been identified to date cannot fully explain the pathogenesis of EV-A71, which is an important global cause of hand, foot, and mouth disease and life-threatening encephalitis. We identified an IFN-γ-inducible EV-A71 cellular entry factor, human tryptophanyl-tRNA synthetase (hWARS), using genome-wide RNAi library screening. The importance of hWARS in mediating virus entry and infectivity was confirmed by virus attachment, in vitro pulldown, antibody/antigen blocking, and CRISPR/Cas9-mediated deletion. Hyperexpression and plasma membrane translocation of hWARS were observed in IFN-γ-treated semipermissive (human neuronal NT2) and cDNA-transfected nonpermissive (mouse fibroblast L929) cells, resulting in their sensitization to EV-A71 infection. Our hWARS-transduced mouse infection model showed pathological changes similar to those seen in patients with severe EV-A71 infection. Expression of hWARS is also required for productive infection by other human enteroviruses, including the clinically important coxsackievirus A16 (CV-A16) and EV-D68. This is the first report to our knowledge on the discovery of an entry factor, hWARS, that can be induced by IFN-γ for EV-A71 infection. Given that we detected high levels of IFN-γ in patients with severe EV-A71 infection, our findings extend the knowledge of the pathogenicity of EV-A71 in relation to entry factor expression upon IFN-γ stimulation and the therapeutic options for treating severe EV-A71-associated complications.
Indexed as
Identifiers
What OpenQuestion holds
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.