Evidence map›Paper›PMID 30755668›Full record

ArticleScientific reports2019

Suppressing the NHEJ pathway by DNA-PKcs inhibitor NU7026 prevents degradation of HBV cccDNA cleaved by CRISPR/Cas9.

Dmitry Kostyushev, Anastasiya Kostyusheva, Sergey Brezgin, Dmitry Zarifyan, Anastasiya Utkina, Irina Goptar, Vladimir Chulanov

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 55 citations in OpenAlex.

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  8. Biologics-based technologies for highly efficient and targeted RNA delivery.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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  14. CRISPR/Cas9 for hepatitis B virus infection treatment.Immunity, inflammation and disease · 2023
    Review
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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 2 institutions in 1 country.

Dmitry KostyushevCentral Research Institute of Epidemiology, Viral Hepatitis, Moscow, 111123, Russian Federation. dk@rcvh.ru.
Anastasiya KostyushevaCentral Research Institute of Epidemiology, Viral Hepatitis, Moscow, 111123, Russian Federation.ORCID 0000-0002-2335-6582
Sergey BrezginCentral Research Institute of Epidemiology, Viral Hepatitis, Moscow, 111123, Russian Federation.
Dmitry ZarifyanCentral Research Institute of Epidemiology, Viral Hepatitis, Moscow, 111123, Russian Federation.
Anastasiya UtkinaCentral Research Institute of Epidemiology, Viral Hepatitis, Moscow, 111123, Russian Federation.
Irina GoptarCentral Research Institute of Epidemiology, Viral Hepatitis, Moscow, 111123, Russian Federation.
Vladimir ChulanovCentral Research Institute of Epidemiology, Viral Hepatitis, Moscow, 111123, Russian Federation.ORCID 0000-0001-6303-9293
Central Research Institute of Epidemiology · RUSechenov University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic hepatitis B is a severe liver disease caused by hepatitis B virus (HBV) infection. Covalently closed circular DNA (cccDNA), a super-spiralized, double-stranded form of the HBV genome, is the major determinant of viral persistence. CRISPR/Cas9 nucleases have been recently shown to introduce double-stranded DNA breaks into HBV cccDNA. The inflicted damage results predominantly in erroneous repair of cccDNA by non-homologous end-joining (NHEJ). NHEJ has been suggested to enhance anti-HBV activity of CRISPR/Cas9 and increase cccDNA mutation. In this study, we assessed anti-HBV activity of CRISPR/Cas9 and cccDNA repair outcomes in an altered NHEJ/HR environment. NU7026, a strong inhibitor of NHEJ, prevented CRISPR/Cas9-mediated degradation of cccDNA and resulted in frequent on-target deletions. We conclude that CRISPR/Cas9 is a highly effective tool to degrade cccDNA and first demonstrate that inhibiting NHEJ impairs cccDNA degradation.

Indexed as

CRISPR-Cas SystemsApoptosisCatalytic DomainCell SurvivalChromonesDNA, CircularDNA End-Joining RepairDNA Mutational AnalysisDNA, ViralGene DeletionGenome, ViralHepatitis B, ChronicHepatitis B virusHep G2 CellsHigh-Throughput Nucleotide SequencingHumans2-(morpholin-4-yl)benzo(h)chromen-4-oneChromonesDNA, CircularDNA, ViralMorpholinesRNA, Guide, CRISPR-Cas Systems

Identifiers

PMID30755668
PMCPMC6372644
OpenAlexW2912162884

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.