ANTIBODY-DEPENDENT ENHANCEMENT OF HIV-1 INFECTION IN HUMAN TERM SYNCYTIOTROPHOBLAST CELLS CULTURED IN-VITRO

We examined if Fc receptor-mediated antibody-dependent enhancement (Fc R-ADE) or complement-mediated antibody-dependent enhancement (C'-ADE) of virus infection can contribute to increasing replication of HIV-1 i n human syncytiotrophoblast (ST) cells. Here we report that both FcR-A DE and C'-ADE may result in enhanced virus release from HIV-1-infected ST cells. We show that FcR-ADE of HIV-1 infection in ST cells is medi ated by FcRIII and other FcR(s) belonging to undetermined Fc classes a nd does not require CD4 receptors, whereas C'-ADE uses both CD4 and CR 2-like receptors. FcR-ADE seems to be more efficient in enhancing HIV- 1 replication than C'-ADE. While FcR-ADE leads to increased internaliz ation of HIV-1, C'-ADE does not result in enhanced endocytosis of the virus. In addition, antibodies mediating FcR-ADE are reactive with the gp120 viral envelope antigen, whereas antibodies involved in C'-ADE r eact with the viral transmembrance glycoprotein gp41. Data suggest tha t both FcR-ADE and C'-ADE may contribute to the spread of HIV-1 from m other to the fetus.