Antibody-dependent enhancement of HIV-1 infection in human term syncytiotrophoblast cells cultured in vitro

SUMMARY We examined if Fc receptor-mediated antibody-dependent enhancement (FcR-ADE) or complement-mediated antibody-dependent enhancement (C′-ADE) of virus infection can contribute to increasing replication of HIV-1 in human syncytiotrophoblast (ST) cells. Here we report that both FcR-ADE and C′-ADE may result in enhanced virus release from HIV-1-infected ST cells. We show that FcR-ADF of HIV-1 infection in ST cells is mediated by FcRIII and other FcR(s) belonging to undetermined Fc classes and does not require CD4 receptors, whereas C'-ADE uses both CD4 and CR2-like receptors. FcR-ADE: seems to be more efficient in enhancing HIV-I replication than C′-ADE. While FcR-ADE leads to increased internalization of HIV-1. C′-ADE does not result in enhanced endocytosis of the virus. In addition, antibodies mediating FcR-ADE arc reactive with the gp120 viral envelope antigen, whereas antibodies involved in C′-ADE react with the viral transmembrane glycoprotein gp41. Data suggest that both FcR-ADH and C′-ADE may contribute lo the spread of HIV-1 from mother to the fetus.