Source:http://linkedlifedata.com/resource/pubmed/id/10201932
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
1999-5-13
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pubmed:abstractText |
Previous studies based on the use of human serum as a source of C have provided evidence for the C-dependent enhancement of cell infection by HIV-1. The present study was undertaken to distinguish C from other serum factors and to identify the proteins and the mechanisms involved in C-dependent cell infection by HIV-1. The classical C activation pathway was reconstituted from the proteins C1q, C1r, C1s, C4, C2, C3, factor H, and factor I; each were purified to homogeneity. A mixture of these proteins at physiological concentrations was shown to reproduce the ability of normal human serum to enhance the infection of MT2 cells by HIV-1 at low doses of virus. This enhancing effect was abolished when heat-inactivated serum and C2- or C3-depleted serum were used, and was restored upon addition of the corresponding purified proteins. A mixture of two synthetic peptides corresponding to positions 10-15 and 90-97 of human C receptor type 2 (CD21) as well as soluble CD4 both inhibited the C-dependent infection process. These data provide unambiguous evidence that HIV-1 triggers a direct activation of the classical C pathway in vitro and thereby facilitates the infection of MT2 cells at low doses of virus. These findings are consistent with a mechanism involving increased interaction between the virus opsonized by C3b-derived fragment(s) and the CD21 cell receptors and subsequent virus entry through CD4 receptors.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Complement C2,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C4,
http://linkedlifedata.com/resource/pubmed/chemical/Complement Factor H,
http://linkedlifedata.com/resource/pubmed/chemical/Complement Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Complement System Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement 3d,
http://linkedlifedata.com/resource/pubmed/chemical/complement factor H, human
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
162
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4088-93
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10201932-Acquired Immunodeficiency Syndrome,
pubmed-meshheading:10201932-Cell Line,
pubmed-meshheading:10201932-Complement C2,
pubmed-meshheading:10201932-Complement C3,
pubmed-meshheading:10201932-Complement C4,
pubmed-meshheading:10201932-Complement Factor H,
pubmed-meshheading:10201932-Complement Factor I,
pubmed-meshheading:10201932-Complement System Proteins,
pubmed-meshheading:10201932-Dose-Response Relationship, Immunologic,
pubmed-meshheading:10201932-Drug Synergism,
pubmed-meshheading:10201932-HIV-1,
pubmed-meshheading:10201932-Humans,
pubmed-meshheading:10201932-Models, Immunological,
pubmed-meshheading:10201932-Receptors, Complement 3d
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pubmed:year |
1999
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pubmed:articleTitle |
In vitro analysis of complement-dependent HIV-1 cell infection using a model system.
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pubmed:affiliation |
Laboratoire d'Enzymologie Moléculaire, Institut de Biologie Structurale, Grenoble, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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