ArticleAntiviral research2016
Susceptibilities of enterovirus D68, enterovirus 71, and rhinovirus 87 strains to various antiviral compounds.
Article in Antiviral research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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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.
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Who cites it
54 citing papers in PubMed, 74 citations in OpenAlex.
- Enterovirus infections in children.Pediatric investigation · 2026Review
- Targeting Picornavirus Nonstructural 2C Protein: Structure, Function, and Antiviral Discovery.ACS infectious diseases · 2026Review
- Establishment of an oral enterovirus 71 (EV71) infection model in immunocompetent mice for antiviral therapy evaluation.Journal of virology · 2026Article
- Comparative immunogenic and structural analysis of virus-like particle and inactivated whole-virion vaccines against enterovirus D68.Molecular therapy. Nucleic acids · 2026Article
- Decoding the complex receptor landscape of enterovirus D68.PLoS pathogens · 2026Review
- Genotype-by-inhibitor interactions to dissect enterovirus replication.Nature communications · 2026Article
- Comparative analysis of deep mutational scanning datasets in enteroviruses A and B identifies functional divergence and therapeutic targets.Nature ecology & evolution · 2026Article
- Rational design and in vivo validation of capsid inhibitors for enterovirus D68.Nature communications · 2026Article
- Respiratory enterovirus D68: virology, clinical surveillance, host-pathogen interactions, and therapeutic prospects.Frontiers in cellular and infection microbiology · 2026Review
- Development of enterovirus transencapsidation assays as tools to understand viral entry.The Journal of general virology · 2025Article
- Genotype-by-Inhibitor Interactions to Dissect Enterovirus Replication.Research square · 2025Article
- Comparative Analysis of Deep Mutational Scanning Datasets in Enteroviruses A and B Identifies Functional Divergence and Therapeutic Targets.Research square · 2025Article
- Review
- Advances in the Treatment of Enterovirus-D68 and Rhinovirus Respiratory Infections.Infectious disease reports · 2025Review
- EV-D68 cleaves LARP1 and PABPC1 by 3Cpro to redirect host mRNA translation machinery toward its genomic RNA.PLoS pathogens · 2025Article
- Novel reporter constructs to accelerate antiviral and therapeutic discovery for Enterovirus-A71.Antiviral research · 2025Article
- Underestimated virus impaired cognition-more evidence and more work to do.Frontiers in immunology · 2025Review
- Emerging Therapeutics in the Fight Against EV-D68: A Review of Current Strategies.Influenza and other respiratory viruses · 2024Review
- Characterization of Effect of Enterovirus D68 in 129/Sv Mice Deficient in IFN-α/β and/or IFN-γ Receptors.Comparative medicine · 2024Article
- Convenient screening of the reproductive toxicity of favipiravir and antiviral drugs inHeliyon · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Compounds were evaluated for antiviral activity in rhabdomyosarcoma (RD) cells against a recent 2014 clinical isolate of enterovirus D68 (EV-D68), a 1962 strain of EV-68D, rhinovirus 87 (RV-87, serologically the same as EV-D68), and enterovirus 71 (EV-71). Test substances included known-active antipicornavirus agents (enviroxime, guanidine HCl, pirodavir, pleconaril, and rupintrivir), nucleobase/nucleoside analogs (3-deazaguanine and ribavirin), and three novel epidithiodiketopiperazines (KCN-2,2'-epi-19, KCN-19, and KCN-21). Of these, rupintrivir was the most potent, with 50% inhibition of viral cytopathic effect (EC50) and 90% inhibition (EC90) of virus yield at 0.0022-0.0053 μM against EV-D68. Enviroxime, pleconaril and the KCN compounds showed efficacy at 0.01-0.3 μM; 3-deazaguanine and pirodavir inhibited EV-D68 at 7-13 μM, and guanidine HCl and ribavirin were inhibitory at 80-135 μM. Pirodavir was active against EV-71 (EC50 of 0.78 μM) but not against RV-87 or EV-D68, and all other compounds were less effective against EV-71 than against RV-87 and EV-D68. The most promising compound inhibiting both virus infections at low concentrations was rupintrivir. Antiviral activity was confirmed for the ten compounds in virus yield reduction (VYR) assays in RD cells, and for enviroxime, guanidine HCl, and pirodavir by cytopathic effect (CPE) assays in A549, HeLa-Ohio-1, and RD cells. These studies may serve as a basis for further pre-clinical discovery of anti-enterovirus inhibitors. Furthermore, the antiviral profiles and growth characteristics observed herein support the assertion that EV-D68 should be classified together with RV-87.
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