ArticleRetrovirology2006
Construction of doxycyline-dependent mini-HIV-1 variants for the development of a virotherapy against leukemias.
Article in Retrovirology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Risks of replication-competent retro/lentivirus from associated vector systems: Is it time for a roadmap toward reduced testing?Molecular therapy. Methods & clinical development · 2025Review
- In-house ELISA protocols for capsid p24 detection of diverse HIV isolates.Virology journal · 2023Article
- HIV-1 3'-Polypurine Tract Mutations Confer Dolutegravir Resistance by Switching to an Integration-Independent Replication Mechanism via 1-LTR Circles.Journal of virology · 2023Article
- Transient CRISPR-Cas Treatment Can Prevent Reactivation of HIV-1 Replication in a Latently Infected T-Cell Line.Viruses · 2021Article
- Role of CXCR4 in the progression and therapy of acute leukaemia.Cell proliferation · 2021Review
- High titers and low fucosylation of early human anti-SARS-CoV-2 IgG promote inflammation by alveolar macrophages.Science translational medicine · 2021Article
- CRISPR-Cas9 Dual-gRNA Attack Causes Mutation, Excision and Inversion of the HIV-1 Proviral DNA.Viruses · 2020Article
- The Impact of HIV-1 Genetic Diversity on CRISPR-Cas9 Antiviral Activity and Viral Escape.Viruses · 2019Article
- The HIV-1 Tat Protein Enhances Splicing at the Major Splice Donor Site.Journal of virology · 2018Article
- Tat-dependent production of an HIV-1 TAR-encoded miRNA-like small RNA.Nucleic acids research · 2016Article
- A short sequence motif in the 5' leader of the HIV-1 genome modulates extended RNA dimer formation and virus replication.The Journal of biological chemistry · 2014Article
- Analysis of partial recombinants in lentiviral vector preparations.Human gene therapy methods · 2014Article
- The allosteric HIV-1 integrase inhibitor BI-D affects virion maturation but does not influence packaging of a functional RNA genome.PloS one · 2014Article
- Opening of the TAR hairpin in the HIV-1 genome causes aberrant RNA dimerization and packaging.Retrovirology · 2012Article
- The HIV-1 Tat protein has a versatile role in activating viral transcription.Journal of virology · 2011Article
- Possible applications for replicating HIV 1 vectors.HIV therapy · 2010Article
- Destabilization of the TAR hairpin leads to extension of the polyA hairpin and inhibition of HIV-1 polyadenylation.Retrovirology · 2009Article
- The 2008 Retrovirology Prize: Ben Berkhout and his RNA world.Retrovirology · 2008Article
- HIV-1 latency in actively dividing human T cell lines.Retrovirology · 2008Article
- The TAR hairpin of human immunodeficiency virus type 1 can be deleted when not required for Tat-mediated activation of transcription.Journal of virology · 2007Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is a high-risk type of blood-cell cancer. We describe the improvement of a candidate therapeutic virus for virotherapy of leukemic cells. Virotherapy is based on the exclusive replication of a virus in leukemic cells, leading to the selective removal of these malignant cells. To improve the safety of such a virus, we constructed an HIV-1 variant that replicates exclusively in the presence of the nontoxic effector doxycycline (dox). This was achieved by replacement of the viral TAR-Tat system for transcriptional activation by the Escherichia coli-derived Tet system for inducible gene expression. This HIV-rtTA virus replicates in a strictly dox-dependent manner. In this virus, additional deletions and/or inactivating mutations were introduced in the genes for accessory proteins. These proteins are essential for virus replication in untransformed cells, but dispensable in leukemic T cells. These minimized HIV-rtTA variants contain up to 7 deletions/inactivating mutations (TAR, Tat, vif, vpR, vpU, nef and U3) and replicate efficiently in the leukemic SupT1 T cell line, but do not replicate in normal peripheral blood mononuclear cells. These virus variants are also able to efficiently remove leukemic cells from a mixed culture with untransformed cells. The therapeutic viruses use CD4 and CXCR4 for cell entry and could potentially be used against CXCR4 expressing malignancies such as T-lymphoblastic leukemia/lymphoma, NK leukemia and some myeloid leukemias.
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