ArticleNature biotechnology2008
Establishment of HIV-1 resistance in CD4+ T cells by genome editing using zinc-finger nucleases.
Article in Nature biotechnology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 562 papers.
What it found
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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.
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.
Who cites it
562 citing papers in PubMed, 997 citations in OpenAlex.
- CCR5-edited CD4+ T cells augment HIV-specific immunity to enable post-rebound control of HIV replication.The Journal of clinical investigation · 2021Trial
- Development of an investigational medicinal stem cell gene therapy product to attempt curing human immunodeficiency virus infection.Scientific reports · 2026Article
- HIV-specific and resistant CAR T cells promote control of HIV replication in people with HIV.Research square · 2026Article
- DisTAL-Seq: A TALEN-specific adaptation of DISCOVER-Seq for off-target profiling.Molecular therapy. Nucleic acids · 2026Article
- Deep learning-driven prediction of on-target activity, off-target risk, and repair outcomes in CRISPR/Cas9: current landscape and multi-scale perspectives.Journal of translational medicine · 2026Review
- BEstimate: a computational tool for the design and interpretation of CRISPR base editing experiments.Genome biology · 2026Article
- CRISPR-based therapeutic genome editing for inherited blood disorders.Nature reviews. Drug discovery · 2025Review
- Engineered Foxp1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Unlocking the role of transcription activator-like effector nuclease (TALENs) and zinc finger nuclease (ZFN) in the treatment of HIV.Molecular biology reports · 2025Review
- Current trends in gene therapy to treat inherited disorders of the brain.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- ATLAS: a rationally designed anterograde transsynaptic tracer.Nature methods · 2025Article
- Turning "trashed" genomic loci into treasurable sites for integrating chimeric antigen receptors in T and NK cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Prime Editing: A Revolutionary Technology for Precise Treatment of Genetic Disorders.Cell proliferation · 2025Review
- Advanced delivery systems for gene editing: A comprehensive review from the GenE-HumDi COST Action Working Group.Molecular therapy. Nucleic acids · 2025Review
- Excision of HIV-1 Provirus in Human Primary Cells with Nanocapsuled TALEN Proteins.ACS applied bio materials · 2025Article
- In pursuit of an HIV cure: from stem cell transplants to gene therapies.Frontiers in genome editing · 2025Review
- Article
- Activation of recombinases at specific DNA loci by zinc-finger domain insertions.Nature biotechnology · 2024Article
- Review
- Cell-Penetrating Peptides and CRISPR-Cas9: A Combined Strategy for Human Genetic Disease Therapy.Human gene therapy · 2024Review
502 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 5 institutions in 2 countries.
Funding
Abstract
Homozygosity for the naturally occurring Delta32 deletion in the HIV co-receptor CCR5 confers resistance to HIV-1 infection. We generated an HIV-resistant genotype de novo using engineered zinc-finger nucleases (ZFNs) to disrupt endogenous CCR5. Transient expression of CCR5 ZFNs permanently and specifically disrupted approximately 50% of CCR5 alleles in a pool of primary human CD4(+) T cells. Genetic disruption of CCR5 provided robust, stable and heritable protection against HIV-1 infection in vitro and in vivo in a NOG model of HIV infection. HIV-1-infected mice engrafted with ZFN-modified CD4(+) T cells had lower viral loads and higher CD4(+) T-cell counts than mice engrafted with wild-type CD4(+) T cells, consistent with the potential to reconstitute immune function in individuals with HIV/AIDS by maintenance of an HIV-resistant CD4(+) T-cell population. Thus adoptive transfer of ex vivo expanded CCR5 ZFN-modified autologous CD4(+) T cells in HIV patients is an attractive approach for the treatment of HIV-1 infection.
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What OpenQuestion holds
Registered trials
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.