Evidence map›Paper›PMID 26334116›Full record

ArticleScientific reports2015

CRISPR/Cas9 nickase-mediated disruption of hepatitis B virus open reading frame S and X.

Madina Karimova, Niklas Beschorner, Werner Dammermann, Jan Chemnitz, Daniela Indenbirken, Jan-Hendrik Bockmann, Adam Grundhoff, Stefan Lüth, Frank Buchholz, Julian Schulze zur Wiesch and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 115 citations in OpenAlex.

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  18. Therapeutic potentials of CRISPR-Cas genome editing technology in human viral infections.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022
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4 more citing papers are in PubMed but not listed here.

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

11 authors at 5 institutions in 1 country.

Madina KarimovaHeinrich Pette Institute - Leibniz Institute for Experimental Virology, 20251 Hamburg, Germany.
Niklas BeschornerHeinrich Pette Institute - Leibniz Institute for Experimental Virology, 20251 Hamburg, Germany.
Werner DammermannDepartment of Medicine I, University Medical Center Eppendorf, 20246 Hamburg, Germany.
Jan ChemnitzHeinrich Pette Institute - Leibniz Institute for Experimental Virology, 20251 Hamburg, Germany.
Daniela IndenbirkenHeinrich Pette Institute - Leibniz Institute for Experimental Virology, 20251 Hamburg, Germany.
Jan-Hendrik BockmannDepartment of Medicine I, University Medical Center Eppendorf, 20246 Hamburg, Germany.
Adam GrundhoffHeinrich Pette Institute - Leibniz Institute for Experimental Virology, 20251 Hamburg, Germany.
Stefan LüthDepartment of Medicine I, University Medical Center Eppendorf, 20246 Hamburg, Germany.
Frank BuchholzDepartment of Medical Systems Biology, University Hospital and Medical Faculty Carl Gustav Carus, TU Dresden, 01307 Dresden, Germany.
Julian Schulze zur WieschDepartment of Medicine I, University Medical Center Eppendorf, 20246 Hamburg, Germany.
Joachim HauberHeinrich Pette Institute - Leibniz Institute for Experimental Virology, 20251 Hamburg, Germany.
Leibniz Institute of Virology (LIV) · DEUniversität Hamburg · DEGerman Center for Infection Research · DEUniversity Hospital Carl Gustav Carus · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current antiviral therapies cannot cure hepatitis B virus (HBV) infection; successful HBV eradication would require inactivation of the viral genome, which primarily persists in host cells as episomal covalently closed circular DNA (cccDNA) and, to a lesser extent, as chromosomally integrated sequences. However, novel designer enzymes, such as the CRISPR/Cas9 RNA-guided nuclease system, provide technologies for developing advanced therapy strategies that could directly attack the HBV genome. For therapeutic application in humans, such designer nucleases should recognize various HBV genotypes and cause minimal off-target effects. Here, we identified cross-genotype conserved HBV sequences in the S and X region of the HBV genome that were targeted for specific and effective cleavage by a Cas9 nickase. This approach disrupted not only episomal cccDNA and chromosomally integrated HBV target sites in reporter cell lines, but also HBV replication in chronically and de novo infected hepatoma cell lines. Our data demonstrate the feasibility of using the CRISPR/Cas9 nickase system for novel therapy strategies aiming to cure HBV infection.

Indexed as

Clustered Regularly Interspaced Short Palindromic RepeatsDeoxyribonuclease IGene SilencingGenome, ViralHepatitis BHepatitis B virusOpen Reading FramesDeoxyribonuclease I

Identifiers

PMID26334116
PMCPMC4558539
OpenAlexW2286337224

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.