Linked Life Data

17164778

Source:http://linkedlifedata.com/resource/pubmed/id/17164778

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pubmed-article:17164778pubmed:abstractTextGene therapy for human immunodeficiency virus (HIV)-1 may be performed by introducing into hematopoietic stem cells genes that inhibit replication of HIV-1 using lentiviral vectors. However, production of lentiviral vectors derived from HIV-1 may be inhibited by the gene being carried to inhibit HIV-1 and these vectors could be mobilized by wild-type HIV-1 infecting transduced cells. This study investigates these problems for the delivery of a dominant-negative rev gene humanized revM10 (huM10) by a lentiviral vector. Although most packaging plasmids suffered inhibition of expression of HIV-1 virion proteins by vectors expressing huM10, the packaging plasmids that expressed the highest levels of HIV-1 virion proteins produced vectors at titers that would be sufficient for clinical applications. The vectors carrying huM10 were used to transduce primary human CD34(+) hematopoietic progenitor cells and yielded high-level transduction without toxicity and conferred potent inhibition of HIV-1. The use of lentiviral vectors with deletion of the enhancers and promoter from the LTR (self-inactivating (SIN) vectors) decreased the frequency of vector mobilization by wild-type HIV-1; SIN vectors carrying huM10 were not mobilized detectably. These studies indicate that lentiviral vectors can be made effective for use in gene therapy for HIV-1.lld:pubmed
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pubmed-article:17164778pubmed:volume15lld:pubmed
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pubmed-article:17164778pubmed:year2007lld:pubmed
pubmed-article:17164778pubmed:articleTitleLentiviral vector transduction of a dominant-negative Rev gene into human CD34+ hematopoietic progenitor cells potently inhibits human immunodeficiency virus-1 replication.lld:pubmed
pubmed-article:17164778pubmed:affiliationDivision of Research Immunology/Bone Marrow Transplantation, The Saban Research Institute of Childrens Hospital Los angeles, Los Angeles, California, USA.lld:pubmed
pubmed-article:17164778pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17164778pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:17164778pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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