ArticleJournal of virology2006
Inhibition of human immunodeficiency virus type 1 replication with artificial transcription factors targeting the highly conserved primer-binding site.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Protein Delivery of Cell-Penetrating Zinc-Finger Activators Stimulates Latent HIV-1-Infected Cells.Molecular therapy. Methods & clinical development · 2020Article
- Reduce and Control: A Combinatorial Strategy for Achieving Sustained HIV Remissions in the Absence of Antiretroviral Therapy.Viruses · 2020Review
- Targeting HIV-1 proviral transcription.Current opinion in virology · 2019Review
- Specific and Stable Suppression of HIV Provirus Expression In Vitro by Chimeric Zinc Finger DNA Methyltransferase 1.Molecular therapy. Nucleic acids · 2017Article
- Genome-Editing Technologies: Principles and Applications.Cold Spring Harbor perspectives in biology · 2016Review
- Specific Reactivation of Latent HIV-1 by dCas9-SunTag-VP64-mediated Guide RNA Targeting the HIV-1 Promoter.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- CRISPR-mediated Activation of Latent HIV-1 Expression.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Article
- Engineering T Cells to Functionally Cure HIV-1 Infection.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Review
- Engineering protocells: prospects for self-assembly and nanoscale production-lines.Life (Basel, Switzerland) · 2015Review
- Designed transcription activator-like effector proteins efficiently induced the expression of latent HIV-1 in latently infected cells.AIDS research and human retroviruses · 2015Article
- Spotting the enemy within: Targeted silencing of foreign DNA in mammalian genomes by the Krüppel-associated box zinc finger protein family.Mobile DNA · 2015Review
- Zinc finger nuclease: a new approach for excising HIV-1 proviral DNA from infected human T cells.Molecular biology reports · 2014Article
- Synthetic zinc finger proteins: the advent of targeted gene regulation and genome modification technologies.Accounts of chemical research · 2014Article
- Specific reactivation of latent HIV-1 with designer zinc-finger transcription factors targeting the HIV-1 5'-LTR promoter.Gene therapy · 2014Article
- Zinc-finger-nucleases mediate specific and efficient excision of HIV-1 proviral DNA from infected and latently infected human T cells.Nucleic acids research · 2013Article
- Molecular Understanding of HIV-1 Latency.Advances in virology · 2012Article
- Proviral HIV-genome-wide and pol-gene specific zinc finger nucleases: usability for targeted HIV gene therapy.Theoretical biology & medical modelling · 2011Article
- Identity of zinc finger nucleases with specificity to herpes simplex virus type II genomic DNA: novel HSV-2 vaccine/therapy precursors.Theoretical biology & medical modelling · 2011Article
- Molecular mechanisms of HIV-1 persistence in the monocyte-macrophage lineage.Retrovirology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
The human immunodeficiency virus type 1 (HIV-1) primer-binding site (PBS) is a highly conserved region in the HIV genome and represents an attractive target for the development of new anti-HIV therapies. In this study, we designed four artificial zinc finger transcription factors to bind at or adjacent to the PBS and repress transcription from the HIV-1 long terminal repeat (LTR). These proteins bound to the LTR in vivo, as demonstrated by the chromatin immunoprecipitation assay. In transient reporter assays, three of the four proteins repressed transcription of a reporter driven by the HIV-1 LTR. Only one of these proteins, however, designated KRAB-PBS2, was able to prevent virus production when transduced into primary lymphocytes. We observed >90% inhibition of viral replication over the course of several weeks compared to untransduced cells, and no significant cytotoxicity was observed. Long-term exposure of HIV-1 to KRAB-PBS2 induced mutations in the HIV-1 PBS that reduced the effectiveness of the repressor, but these mutations also resulted in decreased rates of viral replication. These results show that KRAB-PBS2 has the potential to be used in antiviral therapy for AIDS patients and might complement other gene-based strategies.
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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.