ArticleMolecular therapy : the journal of the American Society of Gene Therapy2014
The impact of unprotected T cells in RNAi-based gene therapy for HIV-AIDS.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- CRISPR-Cas13a Inhibits HIV-1 Infection.Molecular therapy. Nucleic acids · 2020Article
- Influence of a 3' Terminal Ribozyme on AgoshRNA Biogenesis and Activity.Molecular therapy. Nucleic acids · 2019Article
- Review
- Article
- Bone Marrow Gene Therapy for HIV/AIDS.Viruses · 2015Review
- Lentivector Knockdown of CCR5 in Hematopoietic Stem and Progenitor Cells Confers Functional and Persistent HIV-1 Resistance in Humanized Mice.Journal of virology · 2015Article
- The impact of HIV-1 genetic diversity on the efficacy of a combinatorial RNAi-based gene therapy.Gene therapy · 2015Article
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3 authors.
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Abstract
RNA interference (RNAi) is highly effective in inhibiting human immunodeficiency virus type 1 (HIV-1) replication by the expression of antiviral short hairpin RNA (shRNA) in stably transduced T-cell lines. For the development of a durable gene therapy that prevents viral escape, we proposed to combine multiple shRNAs against highly conserved regions of the HIV-1 RNA genome. The future in vivo application of such a gene therapy protocol will reach only a fraction of the T cells, such that HIV-1 replication will continue in the unmodified T cells, thereby possibly frustrating the therapy by generation of HIV-1 variants that escape from the inhibition imposed by the protected cells. We studied virus inhibition and evolution in pure cultures of shRNA-expressing cells versus mixed cell cultures of protected and unprotected T cells. The addition of the unprotected T cells indeed seems to accelerate HIV-1 evolution and escape from a single shRNA inhibitor. However, expression of three antiviral shRNAs from a single lentiviral vector prevents virus escape even in the presence of unprotected cells. These results support the idea to validate the therapeutic potential of this anti-HIV approach in appropriate in vivo models.
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