ArticleMolecular biotechnology2014
A novel approach to block HIV-1 coreceptor CXCR4 in non-toxic manner.
Article in Molecular biotechnology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- HIV cure: from early therapies to cutting-edge strategies.Journal of neurovirology · 2026Review
- New hope and promise with CRISPR-Cas9 technology for the treatment of HIV.Functional & integrative genomics · 2025Review
- Updates on CRISPR-based gene editing in HIV-1/AIDS therapy.Virologica Sinica · 2022Review
- Knowledge From London and Berlin: Finding Threads to a Functional HIV Cure.Frontiers in immunology · 2021Review
- Novel CXCR4 Inhibitor CPZ1344 Inhibits the Proliferation, Migration and Angiogenesis of Glioblastoma.Pathology oncology research : POR · 2020Article
- CCR5 editing by Staphylococcus aureus Cas9 in human primary CD4Retrovirology · 2019Article
- HIV Impacts CD34Frontiers in immunology · 2019Article
- HIV-1 inhibition in cells with CXCR4 mutant genome created by CRISPR-Cas9 and piggyBac recombinant technologies.Scientific reports · 2018Article
- Genome modification of CXCR4 by Staphylococcus aureus Cas9 renders cells resistance to HIV-1 infection.Retrovirology · 2017Article
- Genome editing of CXCR4 by CRISPR/cas9 confers cells resistant to HIV-1 infection.Scientific reports · 2015Article
- Comparison of Lentiviral Packaging Mixes and Producer Cell Lines for RNAi Applications.Molecular biotechnology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chemokine receptor CXCR4 is one of the major coreceptors for human immunodeficiency virus type 1 (HIV-1) and considered as an important therapeutic target. Knockdown of CXCR4 by RNA interference has emerged as a promising strategy for combating HIV-1 infection. However, there is a potential drawback to this strategy as undesired side effects may occur due to the loss of natural function of CXCR4. In this study, we developed a novel approach using a single lentiviral vector to express simultaneously CXCR4 dual-shRNAs and an shRNA-resistant CXCR4 mutant possessing the most possible natural functions of CXCR4 and reduced HIV-1 coreceptor activity. Via this approach we achieved the replacement of endogenous CXCR4 by CXCR4 mutant P191A that could compensate the functional loss of endogenous CXCR4 and significant reduction of HIV-1 replication by 59.2 %. Besides, we demonstrated that construction of recombinant lentiviral vector using 2A peptide-based strategy has significant advantages over using additional promoter-based strategy, including increase of lentivirus titer and avoidance of promoter competition. Therefore, the novel approach to block HIV-1 coreceptor CXCR4 without impairing its normal function provides a new strategy for CXCR4-targeted therapeutics for HIV-1 infection and potential universal applications to knock down a cellular protein in non-toxic manner.
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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.