Linked Life Data

11886260

Source:http://linkedlifedata.com/resource/pubmed/id/11886260

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pubmed-article:11886260pubmed:abstractTextThis report describes induction of HIV-1 resistance and synthesis of resistance factors in immortal CD4-positive T lymphocytes. SupT1 cells were infected by NL4-3 attenuated by a defect in the vif gene through coculture with infected primary lymphocytes. Cell lines from this infection, termed R1, expressed CD4 and CXCR4, carried low levels of HIV-1 DNA, but expressed no other detectable viral products and were resistant to infection by wild-type HIV-1. Investigation of challenge infection in resistant R1 lines demonstrated entry, reverse transcription, and integration by incoming HIV-1 but no synthesis of viral RNA. By assay of marker gene expression, we found that Tat was unable to activate LTR-driven transcription in R1 lines. HIV-1-resistant R1 lines secreted soluble factors that inhibited productive infection of primary lymphocytes by several strains of HIV-1 and blocked viral RNA synthesis in newly infected cells. Resistance factors also blocked the induction of HIV-1 transcription in ACH-2 cells as assayed by viral antigen expression and Northern blot of viral RNA. Soluble factors produced by HIV-1-resistant, immortal R1 cells may form the basis of new approaches to control HIV-1 infection.lld:pubmed
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pubmed-article:11886260pubmed:copyrightInfo(C)2002 Elsevier Science (USA).lld:pubmed
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pubmed-article:11886260pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:11886260pubmed:year2002lld:pubmed
pubmed-article:11886260pubmed:articleTitleInduction of secreted human immunodeficiency virus type 1 (HIV-1) resistance factors in CD4-positive T lymphocytes by attenuated HIV-1 infection.lld:pubmed
pubmed-article:11886260pubmed:affiliationMolecular Virology Division, St. Luke's-Roosevelt Hospital Center, Antenucci Researech Building, 432 West 58th Street, New York, NY 10019, USA.lld:pubmed
pubmed-article:11886260pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11886260pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
pubmed-article:11886260pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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