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.
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.
Giordanengo
V
V
Laboratoire de Virologie, Faculté de Médecine, Centre de Dépistage Anonyme et Gratuit, Hôpital St Roch, Nice, France.
Limouse
M
M
Desroys du Roure
L
L
Cottalorda
J
J
Doglio
A
A
Passeron
A
A
Fuzibet
J G
JG
Lefebvre
J C
JC
D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology; D015703:Antigens, CD; D001172:Arthritis, Rheumatoid / Q000276:immunology; D001323:Autoantibodies / Q000276:immunology*; D001324:Autoantigens / Q000737:chemistry / Q000276:immunology*; D002460:Cell Line; D003429:Cross Reactions; D006031:Glycosylation; D015658:HIV Infections / Q000276:immunology*; D015497:HIV-1; D006509:Hepatitis B / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007075:Immunoglobulin M / Q000276:immunology; D051917:Leukosialin; D008180:Lupus Erythematosus, Systemic / Q000276:immunology; D008970:Molecular Weight; D019158:N-Acetylneuraminic Acid; D012794:Sialic Acids / Q000032:analysis; D012795:Sialoglycoproteins / Q000737:chemistry / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology* / Q000821:virology
D015703:Antigens, CD; D001323:Autoantibodies; D001324:Autoantigens; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D051917:Leukosialin; C465014:SPN protein, human; D012794:Sialic Acids; D012795:Sialoglycoproteins; D019158:N-Acetylneuraminic Acid