Evidence map›Paper›PMID 29773895›Full record

ArticleScientific reports2018

CRISPR/Cas9 system targeting regulatory genes of HIV-1 inhibits viral replication in infected T-cell cultures.

Youdiil Ophinni, Mari Inoue, Tomohiro Kotaki, Masanori Kameoka

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 103 citations in OpenAlex.

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  15. A CRISPR-Cas Cure for HIV/AIDS.International journal of molecular sciences · 2023
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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

4 authors at 2 institutions in 1 country.

Youdiil OphinniCenter for Infectious Diseases, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.ORCID 0000-0001-9443-1538
Mari InoueDepartment of International Health, Kobe University Graduate School of Health Sciences, Hyogo, 654-0142, Japan.
Tomohiro KotakiDepartment of International Health, Kobe University Graduate School of Health Sciences, Hyogo, 654-0142, Japan.
Masanori KameokaCenter for Infectious Diseases, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan. mkameoka@port.kobe-u-ac.jp.ORCID 0000-0001-5525-9915
Hyogo University of Health Sciences · JPKobe University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The CRISPR/Cas9 system provides a novel and promising tool for editing the HIV-1 proviral genome. We designed RNA-guided CRISPR/Cas9 targeting the HIV-1 regulatory genes tat and rev with guide RNAs (gRNA) selected from each gene based on CRISPR specificity and sequence conservation across six major HIV-1 subtypes. Each gRNA was cloned into lentiCRISPRv2 before co-transfection to create a lentiviral vector and transduction into target cells. CRISPR/Cas9 transduction into 293 T and HeLa cells stably expressing Tat and Rev proteins successfully abolished the expression of each protein relative to that in non-transduced and gRNA-absent vector-transduced cells. Tat functional assays showed significantly reduced HIV-1 promoter-driven luciferase expression after tat-CRISPR transduction, while Rev functional assays revealed abolished gp120 expression after rev-CRISPR transduction. The target gene was mutated at the Cas9 cleavage site with high frequency and various indel mutations. Conversely, no mutations were detected at off-target sites and Cas9 expression had no effect on cell viability. CRISPR/Cas9 was further tested in persistently and latently HIV-1-infected T-cell lines, in which p24 levels were significantly suppressed even after cytokine reactivation, and multiplexing all six gRNAs further increased efficiency. Thus, the CRISPR/Cas9 system targeting HIV-1 regulatory genes may serve as a favorable means to achieve functional cures.

Indexed as

CRISPR-Cas SystemsCell LineGenes, revGenes, tatGenetic TherapyHIV-1HumansT-LymphocytesVirus Replication

Identifiers

PMID29773895
PMCPMC5958087
OpenAlexW2804064057

What OpenQuestion holds

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LicenceCC BY
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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.