Antibody-enhanced infection by HIV-1 via Fc receptor-mediated entry
UMass Chan Affiliations
Department of Medicine, Division of Infectious Diseases and ImmunologyCenter for Infectious Disease and Vaccine Research
Document Type
Journal ArticlePublication Date
1988-10-28Keywords
ImmunityImmunology and Infectious Disease
Immunology of Infectious Disease
Infectious Disease
Virology
Metadata
Show full item recordAbstract
Monocytes and macrophages, which may play a central role in the pathogenesis of infection with human immunodeficiency virus type 1 (HIV-1), express the CD4 molecule and Fc receptors (FcR) for immunoglobulin G (IgG). To explore the possibility that FcR mediate HIV-1 infection of monocytes, studies were conducted with the human monocytic cell line U937. These cells were exposed to HIV-1 complexed with various concentrations of serum from HIV-1 antibody-positive individuals and monitored for HIV-1 replication. Serum samples from antibody-negative normal individuals did not affect virus yields. High concentrations of antibody-positive sera showed virus-neutralizing activity; however, cells infected with HIV-1 in the presence of antibody-positive sera at subneutralizing concentrations significantly enhanced virus replication. This infection enhancement was blocked by heat-aggregated gamma-globulin. Moreover, the IgG fraction from an HIV-1 antibody-positive serum enhanced HIV-1 infection at the same serum dilution equivalents. In contrast, IgG-F(ab')2 did not enhance HIV-1 infection but showed neutralizing activity with HIV-1. These results are compatible with the concept of FcR-mediated infection enhancement and suggest that this immunological response to HIV-1, instead of protecting the host, potentially facilitates the infection.Source
Science. 1988 Oct 28;242(4878):580-3. DOI: 10.1126/science.2972065DOI
10.1126/science.2972065Permanent Link to this Item
http://hdl.handle.net/20.500.14038/35131PubMed ID
2972065Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1126/science.2972065