ArticleGene therapy2001
Inhibition of HIV-1 infection by down-regulation of the CXCR4 co-receptor using an intracellular single chain variable fragment against CXCR4.
Article in Gene therapy, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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
15 citing papers in PubMed.
- Applying Antibodies Inside Cells: Principles and Recent Advances in Neurobiology, Virology and Oncology.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2020Review
- Glycosyl-Phosphatidylinositol-Anchored Anti-HIV Env Single-Chain Variable Fragments Interfere with HIV-1 Env Processing and Viral Infectivity.Journal of virology · 2018Article
- Article
- Combined Antiviral Therapy Using Designed Molecular Scaffolds Targeting Two Distinct Viral Functions, HIV-1 Genome Integration and Capsid Assembly.Molecular therapy. Nucleic acids · 2015Article
- Review
- Targeting strategies for delivery of anti-HIV drugs.Journal of controlled release : official journal of the Controlled Release Society · 2014Review
- A simple methodology for conversion of mouse monoclonal antibody to human-mouse chimeric form.Clinical & developmental immunology · 2013Article
- Induction of Kruppel-like factor 5 expression by androgens results in increased CXCR4-dependent migration of prostate cancer cells in vitro.Molecular endocrinology (Baltimore, Md.) · 2009Article
- HIV-1 IN inhibitors: 2010 update and perspectives.Current topics in medicinal chemistry · 2009Review
- Genetic therapies against HIV.Nature biotechnology · 2007Review
- Gene therapy progress and prospects: novel gene therapy approaches for AIDS.Gene therapy · 2005Review
- Inhibition of HIV-1 fusion with small interfering RNAs targeting the chemokine coreceptor CXCR4.Gene therapy · 2004Article
- Protecting from R5-tropic HIV: individual and combined effectiveness of a hammerhead ribozyme and a single-chain Fv antibody that targets CCR5.Gene therapy · 2004Article
- The production and application of single-chain antibody fragments.Folia microbiologica · 2003Review
- Blocking translocation of cell surface molecules from the ER to the cell surface by intracellular antibodies targeted to the ER.Journal of cellular and molecular medicineReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
CXCR4 is the major co-receptor used by X4 strains of human immunodeficiency virus type I (HIV-1). In HIV-1-infected patients, the appearance of X4 strains (T cell line-tropic) correlates with disease progression. Since its discovery, the CXCR4 co-receptor has been a major target for different agents which block its function, such as stromal-derived factor 1alpha (SDF-1alpha) and the anti-CXCR4 monoclonal antibody, 12G5. In the present studies, the 12G5 hybridoma was used to construct a single-chain variable antibody fragment (SFv). Murine leukemia virus (MLV) and simian virus 40 (SV(40)) were utilized as delivery vehicles for the anti-CXCR4 SFv. Intracellular expression of the anti-CXCR4 SFv led to down-regulation of this critical co-receptor, as demonstrated by immunostaining. This effect significantly and specifically protected transduced cells from challenge with HIV-1, as measured by HIV-1 p24 antigen expression. Inhibition of HIV-1 replication was specific for X4 HIV-1 strains as demonstrated by MAGI assays. HeLa-CD4/betagal-CCR5 cells expressing the anti-CXCR4 SFv showed significant inhibition of infectivity by the X4 HIV-1 strain NL4-3, but not with the R5 HIV-1 strain Bal. Thus, this anti-HIV-1 molecular therapy has the potential to inhibit HIV-1 replication and virion spread. Targeting CXCR4 by intracellular immunization could be of additional benefit to certain HIV-1-infected patients on highly active antiretroviral therapy (HAART).
Indexed as
Identifiers
11313818What 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.