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dc.contributor.authorTakeda, Akira
dc.contributor.authorSweet, Raymond W.
dc.contributor.authorEnnis, Francis A.
dc.date2022-08-11T08:09:34.000
dc.date.accessioned2022-08-23T16:36:09Z
dc.date.available2022-08-23T16:36:09Z
dc.date.issued1990-11-01
dc.date.submitted2009-03-26
dc.identifier.citationJ Virol. 1990 Nov;64(11):5605-10.
dc.identifier.issn0022-538X (Print)
dc.identifier.pmid1976824
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38723
dc.description.abstractEvidence 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.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=1976824&dopt=Abstract">Link to Article in PubMed</a>
dc.subjectAntibodies, Monoclonal
dc.subjectAntigens, CD4
dc.subjectAntigens, Differentiation
dc.subjectCD4-Positive T-Lymphocytes
dc.subjectCell Line
dc.subjectEndocytosis
dc.subjectHIV
dc.subjectHIV Antibodies
dc.subjectHIV Infections
dc.subjectHumans
dc.subjectMacrophages
dc.subjectReceptors, Fc
dc.subjectReceptors, IgG
dc.subjectSolubility
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleTwo receptors are required for antibody-dependent enhancement of human immunodeficiency virus type 1 infection: CD4 and Fc gamma R
dc.typeJournal Article
dc.source.journaltitleJournal of virology
dc.source.volume64
dc.source.issue11
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2574&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1575
dc.identifier.contextkey798553
refterms.dateFOA2022-08-23T16:36:09Z
html.description.abstract<p>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.</p>
dc.identifier.submissionpathoapubs/1575
dc.contributor.departmentCenter for Infectious Disease and Vaccine Research
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages5605-10


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