K. Konopka et al., A MONOCLONAL-ANTIBODY TO THE GP120-CD4 COMPLEX HAS DIFFERENTIAL-EFFECTS ON HIV-INDUCED SYNCYTIUM FORMATION AND VIRAL INFECTIVITY, Journal of General Virology, 76, 1995, pp. 669-679
A murine monoclonal antibody (MAb F-91-55) raised against the complex
of soluble CD4 and human immunodeficiency virus type 1 (HIV-1) gp120 h
ad previously been found to inhibit syncytium formation without inhibi
ting the interaction of CD4 with gp120, and its binding site was local
ized within the first two domains (D1/D2) of CD4. We investigated whet
her this antibody inhibited the infectivity of HIV-1 in the CD4(+) T c
ell lines A3.01, Sup-T1 and H9. We also examined the effect of the ant
ibody on syncytium formation between these cells and chronically infec
ted H9 cells. Syncytium formation was found to depend critically on th
e incubation medium used. The effect of the MAb on HIV-1 infectivity w
as very limited with A3.01 and Sup-T1 cells, although it inhibited syn
cytium formation between A3.01 or Sup-T1 and chronically infected H9 c
ells. In contrast, the MAb inhibited significantly the infectivity of
HIV-1 in H9 cells, but it also inhibited syncytium formation between H
9 and chronically infected H9 cells to a greater extent than in the ca
se of the other cell lines. Our results indicate that cellular systems
used for syncytium assays differ in their susceptibility to inhibitor
y 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 ra
ise the possibility that the mechanisms of interaction of gp 120/gp41
with cell membrane CD4 may be different in cell-cell and virus-cell me
mbrane fusion.