7th International AIDS Conference Florence, Italy — June 16-21, 1991

Int Conf AIDS 1991 Jun 16-21; 7:94 (abstract no. M.A.1008)
Kobayashi K, Takeda A, Fanger MW, Ennis FA; Division of Infectious Diseases and Immunology, University of Massachusetts, Worcester, MA

OBJECTIVE: We previously reported that the sera of HIV-1 infected patients have antibodies which enhance infection by HIV-1 of U937 cells and human monocytes (Takeda, A., et al, Science, 1988). Antibody dependent enhancement (ADE) required interaction with both CD4 and Fcalpha receptor (FcalphaR) I (Takeda, A. et al, J. Virol. 1990). This study was designed to evaluate the role of FcalphaR II in ADE of HIV-1 infection.

METHODS: HIV-1 (HTLVIIIB strain) was incubated with mouse anti-HIV-1 gp120 monoclonal antibody (gpI.11.2, IgGl), and then used to infect U937 cells or HeLa cells transfected with genes coding for CD4 and/or FcalphaRII. Infection was measured in culture supernatants of gpI.11.2Fab/IV.3Fab (anti-FcalphaR II) produced by covalently linking the Fab of the mAb to gp120 to the Fab or the mAb to FcalphaR II.

RESULTS: 1) p24 production in U937 cells infected with HIV-1 complexed with the gpI.11.2/IV.3 heteroantibody was significantly (2.1 times) higher than by HIV-1 alone. ADE by the heteroantibody was inhibited by incubation of the cells with aggregated human IgG, indicating ADE was mediated by FcalphaR II. 2) HeLa cells transfected with CD4 and FcalphaR II genes showed increased p24 production when infected with HIV-1 coupled to conventional mAb to gp 120 or to heteroantibody which also contained Fab to FcalphaR II.

CONCLUSIONS: F cR II mediated ADE of HIV-1 infection. CD4 is a required receptor for Fcalpha R II, similar to our results with Fcalpha R I-mediated enhancement of HIV-1 infection.

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