Evidence map›Paper›PMID 23974631›Full record

ArticleScientific reports2013

Harnessing the CRISPR/Cas9 system to disrupt latent HIV-1 provirus.

Hirotaka Ebina, Naoko Misawa, Yuka Kanemura, Yoshio Koyanagi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 308 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
308citing papers in PubMed, 1 pooled it
25.6field-weighted citation impact, top 1% 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

308 citing papers in PubMed, 1 synthesis or guideline pooled it, 564 citations in OpenAlex.

  1. Pooled it
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  9. Searching for a HIV-1 Cure.Theranostics · 2026
    Review
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  12. Article
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248 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

4 authors at 1 institution in 1 country.

Hirotaka EbinaLaboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, 53 Shogoin-kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Naoko Misawa
Yuka Kanemura
Yoshio Koyanagi
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Even though highly active anti-retroviral therapy is able to keep HIV-1 replication under control, the virus can lie in a dormant state within the host genome, known as a latent reservoir, and poses a threat to re-emerge at any time. However, novel technologies aimed at disrupting HIV-1 provirus may be capable of eradicating viral genomes from infected individuals. In this study, we showed the potential of the CRISPR/Cas9 system to edit the HIV-1 genome and block its expression. When LTR-targeting CRISPR/Cas9 components were transfected into HIV-1 LTR expression-dormant and -inducible T cells, a significant loss of LTR-driven expression was observed after stimulation. Sequence analysis confirmed that this CRISPR/Cas9 system efficiently cleaved and mutated LTR target sites. More importantly, this system was also able to remove internal viral genes from the host cell chromosome. Our results suggest that the CRISPR/Cas9 system may be a useful tool for curing HIV-1 infection.

Indexed as

CRISPR-Cas SystemsCRISPR-Associated ProteinsGene SilencingHEK293 CellsHeLa CellsHIV-1HIV Long Terminal RepeatHumansVirus LatencyCRISPR-Associated Proteins

Identifiers

PMID23974631
PMCPMC3752613
OpenAlexW1966452674

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.