ArticleJournal of virology2017
Enterovirus 3A Facilitates Viral Replication by Promoting Phosphatidylinositol 4-Kinase IIIβ-ACBD3 Interaction.
Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 70 citations in OpenAlex.
- Positive-Sense RNA Viruses Reprogramming Membrane Contact Sites to Remodel Organelles and Control Cell Fate.Viruses · 2026Review
- ATG9A is an essential host factor for parechovirus RNA replication.Journal of virology · 2026Article
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- Galectin-9 is a restrictor of infection with multiple enteroviruses.Journal of virology · 2026Article
- Advances in Antiviral Drug Development Targeting Enteroviruses: From Viral Proteins to Host Factors.Viruses · 2026Review
- Reprogramming of lipid metabolism by ORF3a-induced microlipophagy enhances biogenesis of SARS-CoV-2 replication organelle.PLoS pathogens · 2025Article
- Antiviral candidates for enterovirus 71: targeting viral proteome and stage-specific lifecycle interventions.Virology journal · 2025Review
- Plant negative-strand RNA virus phosphoprotein condensates exploit host trafficking and lipid synthesis for viral factory assembly.Science advances · 2025Article
- Hijacking the Host Cell for Replication: Pro-Viral Host Factors Involved in EVA71 Infection.International journal of molecular sciences · 2025Review
- Article
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- Inositol metabolism as a broad-spectrum antiviral target.Frontiers in microbiology · 2025Review
- The multiple roles of viral 3DVirulence · 2024Review
- The class III phosphatidylinositol 3-kinase VPS34 supports EV71 replication by promoting viral replication organelle formation.Journal of virology · 2024Article
- From the "One-Molecule, One-Target, One-Disease" Concept towards Looking for Multi-Target Therapeutics for Treating Non-Polio Enterovirus (NPEV) Infections.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Enterovirus-A71 exploits RAB11 to recruit chaperones for virus morphogenesis.Journal of biomedical science · 2024Article
- Understanding the Neurotrophic Virus Mechanisms and Their Potential Effect on Systemic Lupus Erythematosus Development.Brain sciences · 2024Review
- Multiple functions of the nonstructural protein 3D in picornavirus infection.Frontiers in immunology · 2024Review
- Inhibition of lysosome-tethered Ragulator-Rag-3D complex restricts the replication of Enterovirus 71 and Coxsackie A16.The Journal of cell biology · 2023Article
- Structural insight into EV-A71 3A protein and its interaction with a peptide inhibitor.Virologica Sinica · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Like other enteroviruses, enterovirus 71 (EV71) relies on phosphatidylinositol 4-kinase IIIβ (PI4KB) for genome RNA replication. However, how PI4KB is recruited to the genome replication sites of EV71 remains elusive. Recently, we reported that a host factor, ACBD3, is needed for EV71 replication by interacting with viral 3A protein. Here, we show that ACBD3 is required for the recruitment of PI4KB to RNA replication sites. Overexpression of viral 3A or EV71 infection stimulates the interaction of PI4KB and ACBD3. Consistently, EV71 infection induces the production of phosphatidylinositol-4-phosphate (PI4P). Furthermore, PI4KB, ACBD3, and 3A are all localized to the viral-RNA replication sites. Accordingly, PI4KB or ACBD3 depletion by small interfering RNA (siRNA) leads to a reduction in PI4P production after EV71 infection. I44A or H54Y substitution in 3A interrupts the stimulation of PI4KB and ACBD3. Further analysis suggests that stimulation of ACBD3-PI4KB interaction is also important for the replication of enterovirus 68 but disadvantageous to human rhinovirus 16. These results reveal a mechanism of enterovirus replication that involves a selective strategy for recruitment of PI4KB to the RNA replication sites.
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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.