CD11a/CD18 (LFA-1) epitopes involved in syncytium formation among CD4+ T-cells following cell free HIV-1 infection.

Like particular monoclonal antibodies to CD4, monoclonal antibodies to epitopes localized at the top of the alpha-subunit (CD11a) and at the stem of the beta-subunit (CD18) of the lymphocyte function associated antigen-1 (LFA-1) block syncytium formation when added to CD4+ T-cells before or shortly after (5 min) cell free HIV-1 is added. This indicates involvement of LFA-1 epitopes in the early stage of cell-free infection. Syncytium formation is still blocked by CD4 antibodies when added two hours after virus adsorption, CD11a and CD18 antibodies are ineffective at this late stage. Radio-immune precipitation experiments in acutely infected T-cells with the appropriate CD11a and CD18 antibodies suggested a link between CD18 and CD4 in the cell lines studied, possibly mediated by the CD3/TCR complex. In chronically infected cells, where little CD4 is expressed, LFA-1 antibodies still precipitate the viral envelope, pointing to a direct LFA-1 envelope interaction in that late stage of infection. Our results indicate that a limited number of LFA-1 epitopes is involved in syncytium formation among T-cells, none of which is required for virus entry in the cell or virus spread in the culture.