Open AccessAntibody‐dependent enhancement of HIV‐1 infection in human term syncytiotrophoblast cells cultured in vitro
Author(s) -
TÓTH F. D.,
MOSBORGPETERSEN P.,
KISS J.,
ABOAGYEMATHIESEN G.,
ZDRAVKOVIC M.,
HAGER H.,
ARANYOSI J.,
LAMPÉ L.,
EBBESEN P.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06040.x
Subject(s) - syncytiotrophoblast , immunology , in vitro , antibody , human immunodeficiency virus (hiv) , biology , virology , pregnancy , fetus , placenta , biochemistry , genetics
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.