ArticleCell reports2021
A genome-wide CRISPR screen identifies UFMylation and TRAMP-like complexes as host factors required for hepatitis A virus infection.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
What it found
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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
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- The Post-Transcriptional Regulatory Element of Hepatitis B Virus: From Discovery to Therapy.Viruses · 2024Pooled it
- Narrative review-the emerging role, functions, and mechanisms of UFMylation in cancers.Translational cancer research · 2026Review
- The low-density lipoprotein receptor LDLR mediates cellular entry of nonenveloped hepatitis A virus.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A genus-wide interaction atlas across NS4B orthologues identifies a conserved role for UFMylation in orthoflavivirus replication.Nature communications · 2026Article
- Organoids Gone Viral: A Comprehensive Review on Human Organoid Models to Study Viral Pathogenesis.Viruses · 2026Review
- Review
- Meta-analysis of functional genomics studies reveals conserved cellular pathways required by viruses of pandemic concern.Access microbiology · 2026Article
- Replicon-based genome-wide CRISPR knockout screening for the identification of host factors involved in viral replication.Nature communications · 2025Article
- UFMylation System: Biological Functions, Molecular Mechanisms, Diseases, and Drug Discovery.MedComm · 2025Review
- UFMylation promotes orthoflavivirus infectious particle production.Journal of virology · 2025Article
- Studies on the functional role of UFMylation in cells (Review).Molecular medicine reports · 2025Review
- The many connections of UFMylation with Alzheimer's disease: a comprehensive review.Molecular neurodegeneration · 2025Review
- Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected Cells.Viruses · 2025Article
- Hepato-selective dihydroquinolizinones active against hepatitis A virus in vitro and in vivo.Antiviral research · 2025Article
- Redefining the immune landscape of hepatitis A virus infection.Experimental & molecular medicine · 2025Review
- UFMylation promotes orthoflavivirus infectious particle production.bioRxiv : the preprint server for biology · 2025Article
- Article
- UFMylation: A Potential Modification for Neurological Diseases.Current neuropharmacology · 2025Review
- Hepatovirus translation requires PDGFA-associated protein 1, an eIF4E-binding protein regulating endoplasmic reticulum stress responses.Science advances · 2024Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Hepatitis A virus (HAV) is a positive-sense RNA virus causing acute inflammation of the liver. Here, using a genome-scale CRISPR screen, we provide a comprehensive picture of the cellular factors that are exploited by HAV. We identify genes involved in sialic acid/ganglioside biosynthesis and members of the eukaryotic translation initiation factor complex, corroborating their putative roles for HAV. Additionally, we uncover all components of the cellular machinery for UFMylation, a ubiquitin-like protein modification. We show that HAV translation specifically depends on UFM1 conjugation of the ribosomal protein RPL26. Furthermore, we find that components related to the yeast Trf4/5-Air1/2-Mtr4 polyadenylation (TRAMP) complex are required for viral translation independent of controlling viral poly(A) tails or RNA stability. Finally, we demonstrate that pharmacological inhibition of the TRAMP-like complex decreases HAV replication in hepatocyte cells and human liver organoids, thus providing a strategy for host-directed therapy of HAV 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.