ArticleVirus genes2018
A reverse genetics system for enterovirus D68 using human RNA polymerase I.
Article in Virus genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The trial behind it
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Enterovirus D68 B3 clade strains are efficiently recovered from cDNA infectious clones in 293T cells and infect human spinal cord organoids.Journal of virology · 2026Article
- Review
- EV-D68 cleaves LARP1 and PABPC1 by 3Cpro to redirect host mRNA translation machinery toward its genomic RNA.PLoS pathogens · 2025Article
- The CXCL8/MAPK/hnRNP-K axis enables susceptibility to infection by EV-D68, rhinovirus, and influenza virus in vitro.Nature communications · 2025Article
- Construction of an infectious clone for enterovirus A89 and mutagenesis analysis of viral infection and cell binding.Microbiology spectrum · 2024Article
- Reverse Genetics of Hepatitis C Virus Using an RNA Polymerase I-Mediated Transcription.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Construction and verification of an infectious cDNA clone of coxsackievirus B5.Virologica Sinica · 2022Article
- Pharmacological Characterization of the Mechanism of Action ofACS infectious diseases · 2020Article
- Enzyme-Antibody-Modified Gold Nanoparticle Probes for the Ultrasensitive Detection of Nucleocapsid Protein in SFTSV.International journal of environmental research and public health · 2020Article
- Typical Stress Granule Proteins Interact with the 3' Untranslated Region of Enterovirus D68 To Inhibit Viral Replication.Journal of virology · 2020Article
- A Novel Capsid Binding Inhibitor Displays Potent Antiviral Activity against Enterovirus D68.ACS infectious diseases · 2019Article
- Validating Enterovirus D68-2AJournal of virology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Human enterovirus D68 (EV-D68) is a highly contagious virus, which causes respiratory tract infections. However, no effective vaccines are currently available for controlling EV-D68 infection. Here, we developed a reverse genetics system to recover EV-D68 minireplicons and infectious EV-D68 from transfected plasmids using the RNA polymerase I (Pol I) promoter. The EV-D68 minireplicons contained the luciferase reporter gene, which flanked by the non-coding regions of the EV-D68 RNA. The luciferase signals could be detected in cells after transfection and Pol I promoter-mediated luciferase signal was significantly stronger than that mediated by the T7 promoter. Furthermore, recombinant viruses were generated by transfecting plasmids that contained the genomic RNA segments of EV-D68, under the control of Pol I promoter into 293T cells or RD cells. On plaque morphology and growth kinetics, the rescued virus and parental virus were indistinguishable. In addition, we showed that the G394C mutation disrupts the viral 5'-UTR structure and suppresses the viral cap-independent translation. This reverse genetics system for EV-D68 recovery can greatly facilitate research into EV-D68 biology. Moreover, this system could accelerate the development of EV-D68 vaccines and anti-EV-D68 drugs.
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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.