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(smm)PBj1.9, a molecular clone of SIV(smm)PBj14, induces proliferation of human peripheral blood mononuclear cells (PBMC). We have extended this observation to show that SIV(smm)PBj1.9 induces proliferation of PBMC from pigtailed macaques. This proliferative response was markedly inhibited by mAbs against human class I MHC, class II MHC and CD4 antigens, and partially inhibited by mAbs against integrin β₂ subunit (CD18) and LFA-1 (CD11a). However, these antibodies differed in their ability to inhibit in vitro viral infectivity of PBMC. While anti-CD4, MHC class II, and LFA-1 strongly inhibited viral infectivity, antibodies to MHC class I demonstrated little effect on viral infectivity. A control antibody (PLM2) against porcine CD18 inhibited neither virus-induced proliferation nor viral infectivity. Based on these results, we suggest that SIV(smm)PBj1.9-induced proliferation requires the participation of class I MHC, class II MHC and CD4 molecules. In addition, the observation that anti-class I MHC Ab inhibited proliferation of macaque PBMC induced by mitogen (PHA) and bacterial superantigens, such as Staphylococcus enterotoxin A and toxin shock syndrome toxin-1, suggests that SIV(smm)PBj1.9 also contains a viral superantigen similar to that previously demonstrated in SIV(smm)PBj14.