Evidence map›Paper›PMID 28807685›Full record

ArticleAntiviral research2017

An RNA polymerase II-driven Ebola virus minigenome system as an advanced tool for antiviral drug screening.

Emily V Nelson, Jennifer R Pacheco, Adam J Hume, Tessa N Cressey, Laure R Deflubé, John B Ruedas, John H Connor, Hideki Ebihara, Elke Mühlberger

Open access · greenAbstract read
In one paragraph

Article in Antiviral research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Discovery of three small-molecule inhibitors targetingThe Journal of general virology · 2025
    Article
  3. Article
  4. Marburg Virus Minigenome Assays.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Ebolavirus polymerase uses an unconventional genome replication mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Emily V NelsonDepartment of Microbiology, Boston University School of Medicine, Boston, MA, USA; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA, USA.
Jennifer R PachecoDepartment of Microbiology, Boston University School of Medicine, Boston, MA, USA; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA, USA.
Adam J HumeDepartment of Microbiology, Boston University School of Medicine, Boston, MA, USA; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA, USA.
Tessa N CresseyDepartment of Microbiology, Boston University School of Medicine, Boston, MA, USA; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA, USA.
Laure R DeflubéDepartment of Microbiology, Boston University School of Medicine, Boston, MA, USA; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA, USA.
John B RuedasDepartment of Microbiology, Boston University School of Medicine, Boston, MA, USA; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA, USA.
John H ConnorDepartment of Microbiology, Boston University School of Medicine, Boston, MA, USA; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA, USA.
Hideki EbiharaDepartment of Molecular Medicine, Mayo Clinic, Rochester, MN, USA.
Elke MühlbergerDepartment of Microbiology, Boston University School of Medicine, Boston, MA, USA; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA, USA. Electronic address: muehlber@bu.edu.
Boston University · USMayo Clinic in Arizona · US

Funding

National Center/Emerging Infectous Diseases &BiodefenseUC6AI058618 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MURPHY, JOHN R. · 2003 to 2006
$141.0M
Antiviral responses in iPSC-derived human primary cells to Ebola virus infectionR21AI126457 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MOSTOSLAVSKY, GUSTAVO, MUHLBERGER, ELKE C · 2016 to 2017
$480k
Filovirus replication: initiation mechanism and role of RNA secondary structuresR03AI114293 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MUHLBERGER, ELKE C · 2014 to 2015
$164k
NIAID NIH HHS R03 AI114293NIAID NIH HHS R21 AI126457NIAID NIH HHS UC6 AI058618
6 · The paper itself

Abstract

Ebola virus (EBOV) causes a severe disease in humans with the potential for significant international public health consequences. Currently, treatments are limited to experimental vaccines and therapeutics. Therefore, research into prophylaxis and antiviral strategies to combat EBOV infections is of utmost importance. The requirement for high containment laboratories to study EBOV infection is a limiting factor for conducting EBOV research. To overcome this issue, minigenome systems have been used as valuable tools to study EBOV replication and transcription mechanisms and to screen for antiviral compounds at biosafety level 2. The most commonly used EBOV minigenome system relies on the ectopic expression of the T7 RNA polymerase (T7), which can be limiting for certain cell types. We have established an improved EBOV minigenome system that utilizes endogenous RNA polymerase II (pol II) as a driver for the synthesis of minigenome RNA. We show here that this system is as efficient as the T7-based minigenome system, but works in a wider range of cell types, including biologically relevant cell types such as bat cells. Importantly, we were also able to adapt this system to a reliable and cost-effective 96-well format antiviral screening assay with a Z-factor of 0.74, indicative of a robust assay. Using this format, we identified JG40, an inhibitor of Hsp70, as an inhibitor of EBOV replication, highlighting the potential for this system as a tool for antiviral drug screening. In summary, this updated EBOV minigenome system provides a convenient and effective means of advancing the field of EBOV research.

Indexed as

Genome, ViralAnimalsAntiviral AgentsDNA-Directed RNA PolymerasesEbolavirusHemorrhagic Fever, EbolaHigh-Throughput Screening AssaysHSP72 Heat-Shock ProteinsHumansMicrobial Sensitivity TestsRNA Polymerase IIRNA, ViralTranscription, GeneticViral ProteinsVirus ReplicationAntiviral Agentsbacteriophage T7 RNA polymeraseDNA-Directed RNA PolymerasesHSP72 Heat-Shock ProteinsRNA Polymerase IIRNA, ViralViral ProteinsAntiviral drug screeningEbola virusFilovirusesMinigenome systemRNA polymerase IIT7 RNA polymerase

Identifiers

PMID28807685
PMCPMC5654650
OpenAlexW2742579309

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.