ArticleNature microbiology2019
Enterovirus pathogenesis requires the host methyltransferase SETD3.
Article in Nature microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 86 citations in OpenAlex.
- Respiratory enterovirus D68: virology, clinical surveillance, host-pathogen interactions, and therapeutic prospects.Frontiers in cellular and infection microbiology · 2026Review
- Meta-analysis of functional genomics studies reveals conserved cellular pathways required by viruses of pandemic concern.Access microbiology · 2026Article
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- ARFGAP1 serves as a critical host factor during E30 infection: QS11 inhibits viral pathogenesis in hFcRn-IFNARVirology journal · 2025Article
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- Defining the host dependencies and the transcriptional landscape of RSV infection and bystander activation.bioRxiv : the preprint server for biology · 2025Article
- AlphaFold models of host-pathogen interactions elucidate the prevalence and structural modes of molecular mimicry.bioRxiv : the preprint server for biology · 2025Article
- The methyltransferase SETD3 regulates mRNA alternative splicing through interacting with hnRNPK.Cell insight · 2024Article
- Hepatovirus translation requires PDGFA-associated protein 1, an eIF4E-binding protein regulating endoplasmic reticulum stress responses.Science advances · 2024Article
- Review
- A cytoplasmic form of EHMT1N methylates viral proteins to enable inclusion body maturation and efficient viral replication.PLoS biology · 2024Article
- Baicalein suppresses Coxsackievirus B3 replication by inhibiting caspase-1 and viral protease 2A.Virologica Sinica · 2024Article
- Identification of the proteolytic signature in CVB3-infected cells.Journal of virology · 2024Article
- An efficientJournal of virology · 2024Article
- Gut microbes on the risk of advanced adenomas.BMC microbiology · 2024Article
- The EV71 2A protease occupies the central cleft of SETD3 and disrupts SETD3-actin interaction.Nature communications · 2024Article
- Picornavirus security proteins promote the release of extracellular vesicle enclosed viruses via the modulation of host kinases.PLoS pathogens · 2024Article
- N-terminal acetyltransferase 6 facilitates enterovirus 71 replication by regulating PI4KB expression and replication organelle biogenesis.Journal of virology · 2024Article
- METTL18 functions as a Phenotypic Regulator in Src-Dependent Oncogenic Responses of HER2-Negative Breast Cancer.International journal of biological sciences · 2024Article
Corrections and comments
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Authors and funding
24 authors at 6 institutions in 1 country.
Funding
Abstract
Enteroviruses (EVs) comprise a large genus of positive-sense, single-stranded RNA viruses whose members cause a number of important and widespread human diseases, including poliomyelitis, myocarditis, acute flaccid myelitis and the common cold. How EVs co-opt cellular functions to promote replication and spread is incompletely understood. Here, using genome-scale CRISPR screens, we identify the actin histidine methyltransferase SET domain containing 3 (SETD3) as critically important for viral infection by a broad panel of EVs, including rhinoviruses and non-polio EVs increasingly linked to severe neurological disease such as acute flaccid myelitis (EV-D68) and viral encephalitis (EV-A71). We show that cytosolic SETD3, independent of its methylation activity, is required for the RNA replication step in the viral life cycle. Using quantitative affinity purification-mass spectrometry, we show that SETD3 specifically interacts with the viral 2A protease of multiple enteroviral species, and we map the residues in 2A that mediate this interaction. 2A mutants that retain protease activity but are unable to interact with SETD3 are severely compromised in RNA replication. These data suggest a role of the viral 2A protein in RNA replication beyond facilitating proteolytic cleavage. Finally, we show that SETD3 is essential for in vivo replication and pathogenesis in multiple mouse models for EV infection, including CV-A10, EV-A71 and EV-D68. Our results reveal a crucial role of a host protein in viral pathogenesis, and suggest targeting SETD3 as a potential mechanism for controlling viral infections.
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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.