Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1991-9-19
pubmed:abstractText
The human immunodefiency virus (HIV) uses the human CD4 glycoprotein as a receptor for infection of susceptible cells. Cells expressing a series of mutated forms of the CD4 gene have shown a variability in their ability to support replication of three HIV type 1 (HIV-1) and three HIV-2 strains. Moreover, when different stages of virus production were examined by a variety of assays, a consistent delay was observed in all cell lines containing CD4 mutants compared with those with intact full-length CD4. Cells expressing the CD4.415 mutant (modified at the serine 415 corresponding to a phosphorylation site of the cytoplasmic domain) showed only a minimal effect on virus replication. Cells expressing CD4.403 and CD4.401 mutants (lacking the whole cytoplasmic domain) manifested a moderate delay in production of virus progeny. The most substantial effect on HIV replication was observed in cells expressing a chimeric hybrid containing sequences corresponding to the first 177 residues of the N-terminal CD4 fused to CD8 sequences encoding the hinge, transmembrane, and cytoplasmic domains of the human CD8. Furthermore, in a cell-to-cell contact assay, fusion was absent when the CD4 proximal membrane domain was replaced by the CD8 counterpart. In addition, a strong correlation between the down-modulation of the surface CD4 and HIV expression was observed. These observations suggest that in addition to the known binding region, other domains of CD4 could play an important role in regulating HIV entry of cells.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-1691226, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-1976823, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2109100, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2123627, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2402498, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2413137, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2416116, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2453925, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2454749, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2695168, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2786212, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2830988, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2843773, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2846352, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-2991932, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-3095663, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-3107838, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-3157520, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-3259178, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-3260353, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-3496970, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-3501726, http://linkedlifedata.com/resource/pubmed/commentcorrection/1714523-3629244
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-538X
pubmed:author
pubmed:issnType
Print
pubmed:volume
65
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4893-901
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Several CD4 domains can play a role in human immunodeficiency virus infection in cells.
pubmed:affiliation
Department of Medicine, University of California School of Medicine, San Francisco 94143.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't