ArticleFrontiers in microbiology2018
Caspase-3 Inhibition Attenuates the Cytopathic Effects of EV71 Infection.
Article in Frontiers in microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 30 citations in OpenAlex.
- Serial passagingFrontiers in cellular and infection microbiology · 2026Article
- The EMCV protein 2B* is required for efficient cell lysis via both caspase-3-dependent and -independent pathways during infection.The Journal of general virology · 2025Article
- Advances in anti-EV-A71 drug development research.Journal of advanced research · 2024Review
- Independent role of caspases and Bik in augmenting influenza A virus replication in airway epithelial cells and mice.Virology journal · 2023Article
- Network pharmacology-based exploration identified the antiviral efficacy of Quercetin isolated from mulberry leaves against enterovirus 71 via the NF-κB signaling pathway.Frontiers in pharmacology · 2023Article
- Discovery of New Zika Protease and Polymerase Inhibitors through the Open Science Collaboration Project OpenZika.Journal of chemical information and modeling · 2022Article
- Regulation of host factor γ-H2AX level and location by enterovirus A71 for viral replication.Virulence · 2022Article
- Fucosylated oligosaccharide Lacto-Food chemistry: X · 2022Article
- Total astragalosides decrease apoptosis and pyroptosis by inhibiting enterovirus 71 replication in gastric epithelial cells.Experimental and therapeutic medicine · 2022Article
- Protective Roles of Sodium Butyrate in Lipopolysaccharide-Induced Bovine Ruminal Epithelial Cells by Activating G Protein-Coupled Receptors 41.Frontiers in nutrition · 2022Article
- Autophagy is induced and supports virus replication in Enterovirus A71-infected human primary neuronal cells.Scientific reports · 2020Article
- Caspase-3 inhibitor inhibits enterovirus D68 production.Journal of microbiology (Seoul, Korea) · 2020Article
- [Enterovirus 71 can induce autophagy and apoptosis of THP-1 macrophages].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Cellular Caspase-3 Contributes to EV-A71 2AVirologica Sinica · 2020Article
- Regulation of Apoptosis by Enteroviruses.Frontiers in microbiology · 2020Review
- Coxsackievirus A6 Induces Necroptosis for Viral Production.Frontiers in microbiology · 2020Article
- EV71 3C protease induces apoptosis by cleavage of hnRNP A1 to promote apaf-1 translation.PloS one · 2019Article
- Restriction of H1N1 influenza virus infection by selenium nanoparticles loaded with ribavirin via resisting caspase-3 apoptotic pathway.International journal of nanomedicine · 2018Article
- H5N1 Influenza a Virus Replicates Productively in Pancreatic Cells and Induces Apoptosis and Pro-Inflammatory Cytokine Response.Frontiers in cellular and infection microbiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies demonstrate that human enterovirus 71 (EV71), a primary causative agent for hand, foot, and mouth disease, activates caspase-3 through the non-structural viral 3C protein to induce host cell apoptosis; however, until now it was unclear how 3C activates caspase-3 and how caspase-3 activation affects viral production. Our results demonstrate that 3C binds caspase-8 and caspase-9 but does not directly bind caspase-3 to activate them, and that the proteolytic activity of 3C is required by the activation of caspase-8, caspase-9, and caspase-3. Inhibition of caspase-3 activity attenuates apoptosis in 3C-transfected cells. Furthermore, caspase-3 inhibitor protects host cells from the cytopathic effect of EV71 infection and prevents cell cycle arrest, which is known to be favored for EV71 viral replication. Inhibition of caspase-3 activity decreases EV71 viral protein expression and viral production, but has no effect on viral entry, replication, even polyprotein translation. Therefore, caspase-3 is exploited functionally by EV71 to facilitate its production, which suggests a novel therapeutic approach for the treatment and prevention of hand, foot, and mouth disease.
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.