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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1993-6-25
|
| pubmed:databankReference | |
| pubmed:abstractText |
An HUT-78 cell clone (F12) chronically infected by a nonproducer HIV-1 variant (Federico et al., (1989) AIDS Res. Hum. Retroviruses 5, 385-396) is fully resistant to superinfection with HIV-1 or HIV-2. We demonstrate that, in spite of the down-regulation of CD4 receptors, superinfecting-HIV-1 and -HIV-2 cross the F12 plasma membrane (even in the presence of OKT4A monoclonal antibodies) but fail to complete retrotranscription. We utilized a series of polymerase chain reaction primers designed to detect certain steps in the reverse transcription process. Superinfecting-HIV-1 (an African strain) and -HIV-2 are detectable using primers specific for env (for HIV-1), 5' LTR (the R and U5 regions), and vpx (for HIV-2). No amplification is visible when primers amplifying either HIV-2 gag or the "primer binding site" region of 5' LTR of HIV-2 are used. DNA-PCR performed on DNAse-pretreated HIV-1 and HIV-2 stocks failed to show any amplification. This rules out that any extra- or intravirion viral DNA contamination may have interfered with our results. In addition, no DNA amplification was observed in F12 and HUT-78 cells exposed to heat-inactivated HIV-2. Finally, when the nonproducer F12 cells as well as control CEMss cells are transfected with the HIV-1 infectious molecular clone pNL4-3, progeny infectious virus is obtained. These findings indicate that reverse transcription of HIVs superinfecting F12 cells is prevented from completing viral DNA synthesis. A similar block occurs in HIV-1-infected producer cells. When integration of the HIV genome into the F12 genome is achieved via transfection of a molecular clone, the virus life cycle can proceed as in control CEMss cells.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jun
|
| pubmed:issn |
0042-6822
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
194
|
| pubmed:geneSymbol |
env,
gag
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
441-52
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:8503167-Antigens, CD4,
pubmed-meshheading:8503167-Base Sequence,
pubmed-meshheading:8503167-Clone Cells,
pubmed-meshheading:8503167-DNA, Viral,
pubmed-meshheading:8503167-Down-Regulation,
pubmed-meshheading:8503167-Genes, env,
pubmed-meshheading:8503167-Genes, gag,
pubmed-meshheading:8503167-HIV-1,
pubmed-meshheading:8503167-HIV-2,
pubmed-meshheading:8503167-Humans,
pubmed-meshheading:8503167-Molecular Sequence Data,
pubmed-meshheading:8503167-Polymerase Chain Reaction,
pubmed-meshheading:8503167-Species Specificity,
pubmed-meshheading:8503167-Superinfection,
pubmed-meshheading:8503167-Transcription, Genetic,
pubmed-meshheading:8503167-Transfection,
pubmed-meshheading:8503167-Viral Interference,
pubmed-meshheading:8503167-Virus Replication
|
| pubmed:year |
1993
|
| pubmed:articleTitle |
Homologous superinfection of both producer and nonproducer HIV-infected cells is blocked at a late retrotranscription step.
|
| pubmed:affiliation |
Laboratory of Virology, Istituto Superiore di Sanitá, Rome, Italy.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|