Evidence map›Paper›PMID 20405039›Full record

ArticlePloS one2010

Discovery of selective inhibitors against EBNA1 via high throughput in silico virtual screening.

Ning Li, Scott Thompson, David C Schultz, Weiliang Zhu, Hualiang Jiang, Cheng Luo, Paul M Lieberman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.3field-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

44 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
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  4. Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. In Silico Drug Discovery for Treatment of Virus Diseases.Advances in experimental medicine and biology · 2022
    Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Epstein-Barr virus enhances genome maintenance of Kaposi sarcoma-associated herpesvirus.Proceedings of the National Academy of Sciences of the United States of America · 2018
    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

7 authors at 3 institutions in 2 countries.

Ning LiDrug Discovery and Design Center, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Scott Thompson
David C Schultz
Weiliang Zhu
Hualiang Jiang
Cheng Luo
Paul M Lieberman
Chinese Academy of Sciences · CNThe Wistar Institute · USShanghai Institute of Materia Medica · CN

Funding

Regulation of Epstein-Barr Virus LatencyR01CA093606 · NCI · WISTAR INSTITUTE · PI LIEBERMAN, PAUL M. · 2002 to 2022
$6.7M
Assay For Inhibitors of Epstein-Barr VirusR21NS063906 · NINDS · WISTAR INSTITUTE · PI LIEBERMAN, PAUL M. · 2008 to 2009
$193k
NCI NIH HHS R01 CA093606NCI NIH HHS R01CA093606NINDS NIH HHS R21 NS063906NINDS NIH HHS R21NS063906
6 · The paper itself

Abstract

backgroundEpstein-Barr Virus (EBV) latent infection is associated with several human malignancies and is a causal agent of lymphoproliferative diseases during immunosuppression. While inhibitors of herpesvirus DNA polymerases, like gancyclovir, reduce EBV lytic cycle infection, these treatments have limited efficacy for treating latent infection. EBNA1 is an EBV-encoded DNA-binding protein required for viral genome maintenance during latent infection. METHODOLOGY: Here, we report the identification of a new class of small molecules that inhibit EBNA1 DNA binding activity. These compounds were identified by virtual screening of 90,000 low molecular mass compounds using computational docking programs with the solved crystal structure of EBNA1. Four structurally related compounds were found to inhibit EBNA1-DNA binding in biochemical assays with purified EBNA1 protein. Compounds had a range of 20-100 microM inhibition of EBNA1 in fluorescence polarization assays and were further validated for inhibition using electrophoresis mobility shift assays. These compounds exhibited no significant inhibition of an unrelated DNA binding protein. Three of these compounds inhibited EBNA1 transcription activation function in cell-based assays and reduced EBV genome copy number when incubated with a Burkitt lymphoma cell line.

conclusionsThese experiments provide a proof-of-principle that virtual screening can be used to identify specific inhibitors of EBNA1 that may have potential for treatment of EBV latent infection.

Indexed as

Burkitt LymphomaCell Line, TumorComputer SimulationDNADrug DiscoveryDrug Evaluation, PreclinicalEpstein-Barr Virus InfectionsEpstein-Barr Virus Nuclear AntigensHerpesvirus 4, HumanHumansProtein BindingTranscription, GeneticViral ProteinsDNAEBV-encoded nuclear antigen 1Epstein-Barr Virus Nuclear AntigensViral Proteins

Identifiers

PMID20405039
PMCPMC2853575
OpenAlexW2058743222

What OpenQuestion holds

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Registered trials

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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.