Evidence map›Paper›PMID 37346975›Full record

ArticleMolecular therapy. Nucleic acids2023

Strategic self-limiting production of infectious HIV particles by CRISPR in permissive cells.

Hong Liu, Chen Chen, Shuren Liao, Danielle K Sohaii, Conrad R Y Cruz, Tricia H Burdo, Thomas J Cradick, Anand Mehta, Carlos Barrero, Magda Florez and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy. Nucleic acids, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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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

17 authors at 3 institutions in 1 country.

Hong LiuCenter for Neurovirology and Gene Editing, Department of Microbiology, Immunology, and Inflammation, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, 7th Floor, Philadelphia, PA 19140, USA.
Chen ChenCenter for Neurovirology and Gene Editing, Department of Microbiology, Immunology, and Inflammation, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, 7th Floor, Philadelphia, PA 19140, USA.
Shuren LiaoCenter for Neurovirology and Gene Editing, Department of Microbiology, Immunology, and Inflammation, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, 7th Floor, Philadelphia, PA 19140, USA.
Danielle K SohaiiCenter for Cancer and Immunology Research, Children's National Health System, The George Washington University, 7144 13th Place NW, Washington, DC 20012, USA.
Conrad R Y CruzCenter for Cancer and Immunology Research, Children's National Health System, The George Washington University, 7144 13th Place NW, Washington, DC 20012, USA.
Tricia H BurdoCenter for Neurovirology and Gene Editing, Department of Microbiology, Immunology, and Inflammation, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, 7th Floor, Philadelphia, PA 19140, USA.
Thomas J CradickExcision Biotherapeutics, Inc., 499 Jackson Street, San Francisco, CA 94111, USA.
Anand MehtaDepartment of Cell and Molecular Pharmacology, Medical University of South Carolina, Basic Science Building, Room 310, 173 Ashley Avenue, Charleston, SC 29425, USA.
Carlos BarreroDepartment of Pharmaceutical Sciences, School of Pharmacy, Temple University, 3307 N. Broad Street, Philadelphia, PA 19140, USA.
Magda FlorezDepartment of Pharmaceutical Sciences, School of Pharmacy, Temple University, 3307 N. Broad Street, Philadelphia, PA 19140, USA.
Jennifer GordonExcision Biotherapeutics, Inc., 499 Jackson Street, San Francisco, CA 94111, USA.
Stephane GrauzamDepartment of Cell and Molecular Pharmacology, Medical University of South Carolina, Basic Science Building, Room 310, 173 Ashley Avenue, Charleston, SC 29425, USA.
James DressmanDepartment of Cell and Molecular Pharmacology, Medical University of South Carolina, Basic Science Building, Room 310, 173 Ashley Avenue, Charleston, SC 29425, USA.
Shohreh AminiDepartment of Biology, College of Science and Technology, Temple University, 1900 North 12th Street, Philadelphia, PA 19122, USA.
Catherine M BollardCenter for Cancer and Immunology Research, Children's National Health System, The George Washington University, 7144 13th Place NW, Washington, DC 20012, USA.
Rafal KaminskiCenter for Neurovirology and Gene Editing, Department of Microbiology, Immunology, and Inflammation, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, 7th Floor, Philadelphia, PA 19140, USA.
Kamel KhaliliCenter for Neurovirology and Gene Editing, Department of Microbiology, Immunology, and Inflammation, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, 7th Floor, Philadelphia, PA 19140, USA.
Temple University · USChildren's National · USMedical University of South Carolina · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-translational glycosylation of the HIV-1 envelope protein involving precursor glycan trimming by mannosyl oligosaccharide glucosidase (MOGS) is critically important for morphogenesis of virions and viral entry. Strategic editing of the MOGS gene in T lymphocytes and myeloid origin cells harboring latent proviral DNA results in the production of non-infectious particles upon treatment of cells with latency reversal agents. Controlled activation of CRISPR-MOGS by rebound HIV-1 mitigates production of infectious particles that exhibit poor ability of the virus to penetrate uninfected cells. Moreover, exclusive activation of CRISPR in cells infected with HIV-1 alleviates concern for broad off-target impact of MOGS gene ablation in uninfected cells. Combination CRISPR treatment of peripheral blood lymphocytes prepared from blood of people with HIV-1 (PWH) tailored for editing the MOGS gene (CRISPR-MOGS) and proviral HIV-1 DNA (CRISPR-HIV) revealed a cooperative impact of CRISPR treatment in inhibiting the production of infectious HIV-1 particles. Our design for genetic inactivation of MOGS by CRISPR exhibits no detectable off-target effects on host cells or any deleterious impact on cell survival and proliferation. Our findings offer the development of a new combined gene editing-based cure strategy for the diminution of HIV-1 spread after cessation of antiretroviral therapy (ART) and its elimination.

Indexed as

combined gene editing for HIV cureCRISPR gene editingCRISPR prevention of viral entryglycosylationHIV infectionmannosyl oligosaccharide glucosidase (MOGS)MT: RNA/DNA Editingnon-infectious virus production

Identifiers

PMID37346975
PMCPMC10280355
OpenAlexW4377092189

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.