ANTIBODY TO HUMAN MHC CLASS-I INHIBITS SIV(SMM)PBJ1.9-INDUCED PROLIFERATION OF PIGTAILED MACAQUE LYMPHOCYTES

Previously we have shown that the simian immunodeficiency virus SIV(sm m)PBj1.9, a molecular clone of SIV(smm)PBj14, induces proliferation of human peripheral blood mononuclear cells (PBMC). We have extended thi s observation to show that SIV(smm)PBj1.9 induces proliferation of PBM C from pigtailed macaques. This proliferative response was markedly in hibited by mAbs against human class I MHC, class II MHC and CD4 antige ns, and partially inhibited by mAbs against integrin beta(2) subunit ( CD18) and LFA-1 (CD11a). However, these antibodies differed in their a bility to inhibit in vitro viral infectivity of PBMC. While anti-CD4, MHC class II, and LFA-1 strongly inhibited viral infectivity, antibodi es to MHC class I demonstrated little effect on viral infectivity. A c ontrol antibody (PLM2) against porcine CD18 inhibited neither virus-in duced proliferation nor viral infectivity. Based on these results, we suggest that SIV(smm)PBj1.9-induced proliferation requires the partici pation of class I MHC, class II MHC and CD4 molecules. In addition, th e observation that anti-class I MHC Ab inhibited proliferation of maca que PBMC induced by mitogen (PHA) and bacterial superantigens, such as Staphylococcus enterotoxin A and toxin shock syndrome toxin-l, sugges ts that SIV(smm)PBj1.9 also contains a viral superantigen similar to t hat previously demonstrated in SIV(smm)PBj14.