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A monoclonal antibody to the gp120-CD4 complex has differential effects on HIV-induced syncytium formation and viral infectivity

Nejat Düzgüne^1,3,*

¹ Department of Microbiology, University of the Pacific, School of Dentistry, San Francisco, CA 94115
² Institute for Molecular Immunology, Hospital for Joint Diseases, New York University, New York, NY 10003
and³ Department of Pharmacy, School of Pharmacy, University of California, San Francisco, CA 94143, USA

A murine monoclonal antibody (MAb F-91-55) raised against the complex of soluble CD4 and human immunodeficiency virus type 1 (HIV-1) gp120 had previously been found to inhibit syncytium formation without inhibiting the interaction of CD4 with gp120, and its binding site was localized within the first two domains (D1/D2) of CD4. We investigated whether this antibody inhibited the infectivity of HIV-1 in the CD4⁺ T cell lines A3.01, Sup-T1 and H9. We also examined the effect of the antibody on syncytium formation between these cells and chronically infected H9 cells. Syncytium formation was found to depend critically on the incubation medium used. The effect of the MAb on HIV-1 infectivity was very limited with A3.01 and Sup-T1 cells, although it inhibited syncytium formation between A3.01 or Sup-T1 and chronically infected H9 cells. In contrast, the MAb inhibited significantly the infectivity of HIV-1 in H9 cells, but it also inhibited syncytium formation between H9 and chronically infected H9 cells to a greater extent than in the case of the other cell lines. Our results indicate that cellular systems used for syncytium assays differ in their susceptibility to inhibitory antibodies. In the A3.01 and Sup-T1 cell systems, the differences in the ability of the MAb to block viral entry or syncytium formation raise the possibility that the mechanisms of interaction of gp120/gp41 with cell membrane CD4 may be different in cell-cell and virus-cell membrane fusion.

^* Author for correspondence [mail should be sent to address (1)]. Fax +1 415 929 6564. e-mail nejat@itsa.ucsf.edu

Received 22 July 1994; accepted 24 October 1994.

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