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rdf:type |
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lifeskim:mentions |
umls-concept:C0019704,
umls-concept:C0021311,
umls-concept:C0282632,
umls-concept:C0597357,
umls-concept:C1332714,
umls-concept:C1514873,
umls-concept:C1546857,
umls-concept:C1552644,
umls-concept:C1556066,
umls-concept:C1619636,
umls-concept:C1823153,
umls-concept:C2349976
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pubmed:issue |
11
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pubmed:dateCreated |
1990-11-15
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pubmed:abstractText |
Evidence of antibody-dependent enhancement of human immunodeficiency virus type 1 (HIV-1) infection via Fc receptor (FcR) was published previously (A. Takeda, C. U. Tuazon, and F. A. Ennis, Science 242:580-583, 1988). To define the entry mechanism of HIV-1 complexed with anti-HIV-1 antibody, we attempted to determine the receptor molecules responsible for mediating enhancement of HIV-1 infection of monocytic cells. Monoclonal antibodies to FcRI for immunoglobulin G substantially blocked antibody-dependent enhancement of HIV-1 infection. Furthermore, we demonstrate a requirement for the CD4 molecule in antibody-enhanced HIV-1 infection via FcR. Soluble CD4 prevented infection by HIV-1 antibody-treated virus, and enhancement of infection of virus-antibody complexes was abrogated by a monoclonal antibody to CD4 (anti-Leu3a antibody). Treatment of human macrophages with an anti-CD4 antibody also inhibited antibody-enhanced HIV-1 infection of macrophages, supporting our contention that antibody-dependent enhancement of HIV-1 infection via FcR requires CD4 interaction with the virus glycoprotein.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2139079,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2324685,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2430333,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2459406,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2474608,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2523711,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2536142,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2554488,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2786088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2786212,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2786647,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2895317,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2897548,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2936805,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2972065,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-2981931,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-3107838,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-3257544,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-3262112,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-6083454,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-6096719,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-6854270,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-7251133,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1976824-7252155
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/HIV Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Fc,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgG
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-538X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
64
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5605-10
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:1976824-Antibodies, Monoclonal,
pubmed-meshheading:1976824-Antigens, CD4,
pubmed-meshheading:1976824-Antigens, Differentiation,
pubmed-meshheading:1976824-CD4-Positive T-Lymphocytes,
pubmed-meshheading:1976824-Cell Line,
pubmed-meshheading:1976824-Endocytosis,
pubmed-meshheading:1976824-HIV,
pubmed-meshheading:1976824-HIV Antibodies,
pubmed-meshheading:1976824-HIV Infections,
pubmed-meshheading:1976824-Humans,
pubmed-meshheading:1976824-Macrophages,
pubmed-meshheading:1976824-Receptors, Fc,
pubmed-meshheading:1976824-Receptors, IgG,
pubmed-meshheading:1976824-Solubility
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pubmed:year |
1990
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pubmed:articleTitle |
Two receptors are required for antibody-dependent enhancement of human immunodeficiency virus type 1 infection: CD4 and Fc gamma R.
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pubmed:affiliation |
Department of Medicine, University of Massachusetts Medical School, Worcester 01655.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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