UMMS Affiliation

Department of Medicine, Division of Infectious Diseases and Immunology; Center for Infectious Disease and Vaccine Research

Publication Date

11-1-1990

Document Type

Article

Subjects

Antibodies, Monoclonal; Antigens, CD4; Antigens, Differentiation; CD4-Positive T-Lymphocytes; Cell Line; Endocytosis; HIV; HIV Antibodies; HIV Infections; Humans; Macrophages; Receptors, Fc; Receptors, IgG; Solubility

Disciplines

Life Sciences | Medicine and Health Sciences

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.

Rights and Permissions

Citation: J Virol. 1990 Nov;64(11):5605-10.

Related Resources

Link to Article in PubMed

Journal/Book/Conference Title

Journal of virology

PubMed ID

1976824

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