pubmed-article:9371653 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9371653 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
pubmed-article:9371653 | lifeskim:mentions | umls-concept:C0086962 | lld:lifeskim |
pubmed-article:9371653 | lifeskim:mentions | umls-concept:C0009013 | lld:lifeskim |
pubmed-article:9371653 | lifeskim:mentions | umls-concept:C0376705 | lld:lifeskim |
pubmed-article:9371653 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
pubmed-article:9371653 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
pubmed-article:9371653 | lifeskim:mentions | umls-concept:C0333668 | lld:lifeskim |
pubmed-article:9371653 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:9371653 | pubmed:dateCreated | 1997-12-24 | lld:pubmed |
pubmed-article:9371653 | pubmed:abstractText | The posttranscriptional control element CTE of the simian type D retrovirus has been shown to support replication of Rev-Rev-responsive-element (RRE)-deficient molecular clones of human immunodeficiency virus type 1 (HIV-1). Upon infection of peripheral blood mononuclear cells in vitro, these CTE-containing Rev-independent viruses that are nef+ or nef-minus showed lower replicative capacity and infectivity than the wild-type HIV-1. We studied the effects of Rev-RRE replacement by the CTE on HIV-1 expression with SCID-hu mice. The nef+ and nef-minus Rev-independent viruses established infection with kinetics slower than that of the nef-minus NL4-3. Most importantly, no depletion of CD4-bearing thymocytes was observed after 6 weeks for mice infected with these Rev-independent viruses. This is in contrast to the infection with both wild-type and nef-minus viruses, which led to varying depletion of thymocytes. These data suggest an attenuated phenotype for growth and cytotoxicity of the Rev-independent HIV-1 clones in SCID-hu mice, independent of the presence of Nef. The mutant viruses, which have the essential Rev-RRE regulatory system eliminated, display a distinct phenotype not previously observed with HIV mutant viruses having deletions of accessory genes. Therefore, replacement of the Rev-RRE regulatory axis may generate viruses with altered biological properties in vivo. | lld:pubmed |
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pubmed-article:9371653 | pubmed:language | eng | lld:pubmed |
pubmed-article:9371653 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9371653 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:9371653 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9371653 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9371653 | pubmed:month | Dec | lld:pubmed |
pubmed-article:9371653 | pubmed:issn | 0022-538X | lld:pubmed |
pubmed-article:9371653 | pubmed:author | pubmed-author:PavlakisG NGN | lld:pubmed |
pubmed-article:9371653 | pubmed:author | pubmed-author:FelberB KBK | lld:pubmed |
pubmed-article:9371653 | pubmed:author | pubmed-author:ValentinAA | lld:pubmed |
pubmed-article:9371653 | pubmed:author | pubmed-author:ZackJ AJA | lld:pubmed |
pubmed-article:9371653 | pubmed:author | pubmed-author:ColeS WSW | lld:pubmed |
pubmed-article:9371653 | pubmed:author | pubmed-author:ZolotukhinA... | lld:pubmed |
pubmed-article:9371653 | pubmed:author | pubmed-author:AldrovandiGG | lld:pubmed |
pubmed-article:9371653 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9371653 | pubmed:volume | 71 | lld:pubmed |
pubmed-article:9371653 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9371653 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9371653 | pubmed:pagination | 9817-22 | lld:pubmed |
pubmed-article:9371653 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:9371653 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9371653 | pubmed:articleTitle | Reduced viral load and lack of CD4 depletion in SCID-hu mice infected with Rev-independent clones of human immunodeficiency virus type 1. | lld:pubmed |
pubmed-article:9371653 | pubmed:affiliation | ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201, USA. | lld:pubmed |
pubmed-article:9371653 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9371653 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:9371653 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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