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Autoantibodies directed against CD43 molecules with an altered
glycosylation status on human immunodeficiency virus type 1 (HIV-1)-
infected CEM cells are found in all HIV-1+ individuals
V Giordanengo, M Limouse, L Desroys du Roure, J Cottalorda, A Doglio, A Passeron, JG Fuzibet and JC Lefebvre
Laboratoire de Virologie, Faculte de Medecine, Centre de Depistage Anonyme
et Gratuit, Hopital St Roch, Nice, France.
Autoantibodies to lymphocytes have been detected in sera from human
immunodeficiency virus type 1 (HIV-1)-infected individuals, and several
autoantigens have been described. Among them, hyposialylated CD43 has been
shown to be a target for autoantibodies in up to 47% of HIV+ individuals.
However, the corresponding autoantigen (ie, the incompletely sialylated
CD43) has not been isolated from blood cells of HIV-1-infected individuals.
Recently, we have observed in vitro that HIV-1 productively or latently
infected CEM cells (CEMLAI/NP) express CD43 molecules with modified
glycosylation (mogly CD43). Using CEMLAI/NP cells, which do not express any
structural viral antigen, we show now that all of the tested HIV+ sera from
asymptomatic individuals, and up to 86% of those from subjects at the
acquired immunodeficiency syndrome stage contain antibodies (mainly IgM
and, to a lesser degree, IgG) that recognize the surface of CEMLAI/NP
cells, and precipitate mogly CD43 molecules from the cells lysates. Taken
together with our previous demonstration of altered glycosylation of CD43
from HIV-1-infected CEM cells in vitro, the constant antimogly CD43
autoimmune response observed from asymptomatic HIV-1+ subjects is likely to
illustrate the occurrence of an altered glycosylation in vivo of the major
lymphocyte surface CD43 glycoprotein, associated with HIV- 1 infection.
Volume 86,
Issue 6,
pp. 2302-2311,
09/15/1995
Copyright © 1995 by The American Society of Hematology
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