Antibody-dependent enhancement of HIV-1 infection in human term syncytiotrophoblast cells cultured in vitro.
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-ADE 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-1 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 are 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-ADE and C'-ADE may contribute to the spread of HIV-1 from mother to the fetus.
Tóth
F D
FD
Danish Cancer Society, Department of Virus and Cancer, Aarhus.
Mosborg-Petersen
P
P
Kiss
J
J
Aboagye-Mathiesen
G
G
Zdravkovic
M
M
Hager
H
H
Aranyosi
J
J
Lampé
L
L
Ebbesen
P
P
D002478:Cells, Cultured; D003165:Complement System Proteins / Q000276:immunology; D005260:Female; D015483:HIV Antibodies; D015658:HIV Infections / Q000150:complications / Q000276:immunology* / Q000635:transmission; D015497:HIV-1 / Q000276:immunology / Q000502:physiology; D006801:Humans; D008431:Maternal-Fetal Exchange; D009500:Neutralization Tests; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology / Q000382:microbiology; D011961:Receptors, Fc / Q000276:immunology; D014327:Trophoblasts / Q000382:microbiology*; D014779:Virus Replication / Q000276:immunology
D015483:HIV Antibodies; D011961:Receptors, Fc; D003165:Complement System Proteins