Two receptors are required for antibody-dependent enhancement of human immunodeficiency virus type 1 infection: CD4 and Fc gamma R
dc.contributor.author | Takeda, Akira | |
dc.contributor.author | Sweet, Raymond W. | |
dc.contributor.author | Ennis, Francis A. | |
dc.date | 2022-08-11T08:09:34.000 | |
dc.date.accessioned | 2022-08-23T16:36:09Z | |
dc.date.available | 2022-08-23T16:36:09Z | |
dc.date.issued | 1990-11-01 | |
dc.date.submitted | 2009-03-26 | |
dc.identifier.citation | J Virol. 1990 Nov;64(11):5605-10. | |
dc.identifier.issn | 0022-538X (Print) | |
dc.identifier.pmid | 1976824 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/38723 | |
dc.description.abstract | 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. | |
dc.language.iso | en_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.subject | Antibodies, Monoclonal | |
dc.subject | Antigens, CD4 | |
dc.subject | Antigens, Differentiation | |
dc.subject | CD4-Positive T-Lymphocytes | |
dc.subject | Cell Line | |
dc.subject | Endocytosis | |
dc.subject | HIV | |
dc.subject | HIV Antibodies | |
dc.subject | HIV Infections | |
dc.subject | Humans | |
dc.subject | Macrophages | |
dc.subject | Receptors, Fc | |
dc.subject | Receptors, IgG | |
dc.subject | Solubility | |
dc.subject | Life Sciences | |
dc.subject | Medicine and Health Sciences | |
dc.title | Two receptors are required for antibody-dependent enhancement of human immunodeficiency virus type 1 infection: CD4 and Fc gamma R | |
dc.type | Journal Article | |
dc.source.journaltitle | Journal of virology | |
dc.source.volume | 64 | |
dc.source.issue | 11 | |
dc.identifier.legacyfulltext | https://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2574&context=oapubs&unstamped=1 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/oapubs/1575 | |
dc.identifier.contextkey | 798553 | |
refterms.dateFOA | 2022-08-23T16:36:09Z | |
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.submissionpath | oapubs/1575 | |
dc.contributor.department | Center for Infectious Disease and Vaccine Research | |
dc.contributor.department | Department of Medicine, Division of Infectious Diseases and Immunology | |
dc.source.pages | 5605-10 |