Search

Your search keyword '"Chehadeh, Wassim"' showing total 70 results
Start Over Author "Chehadeh, Wassim"
70 results on '"Chehadeh, Wassim"'

54. Novel NSP4 genotype in a camel G10P[15] rotavirus strain

Author

Papp, Hajnalka, primary, Al-Mutairi, Laila, additional, Chehadeh, Wassim, additional, Farkas, Szilvia, additional, Lengyel, György, additional, Jakab, Ferenc, additional, Martella, Vito, additional, Szűcs, György, additional, and Bányai, Krisztián, additional

Published
2012
Full Text
View/download PDF

59. A part of the VP4 capsid protein exhibited by coxsackievirus B4 E2 is the target of antibodies contained in plasma from patients with type 1 diabetes

Author

Sauter, Pierre, primary, Chehadeh, Wassim, additional, Lobert, Pierre-Emmanuel, additional, Lazrek, Mouna, additional, Goffard, Anne, additional, Soumillon, Magalie, additional, Caloone, Delphine, additional, Vantyghem, Marie-Christine, additional, Weill, Jacques, additional, Fajardy, Isabelle, additional, Alm, Gunnar, additional, Lucas, Bernadette, additional, and Hober, Didier, additional

Published
2008
Full Text
View/download PDF

68. Persistent Infection of Human Pancreatic Islets by Coxsackievirus B Is Associated with Alpha Interferon Synthesis in ß Cells

Author

Chehadeh, Wassim, Kerr-Conte, Julie, Pattou, Franc¸ois, Alm, Gunar, Lefebvre, Jean, Wattre´, Pierre, and Hober, Didier

Abstract

ABSTRACTThe interactions of coxsackievirus B3 (CVB3), CVB4E2 (diabetogenic), and CVB4JBV (nondiabetogenic) strains with human pancreatic islets from eight adult brain-dead donors were investigated. Persistent replication of viruses in human islets was proved by detection of viral RNA by in situ hybridization, VP1 capsid protein by immunofluorescence (IF) staining, negative-strand viral RNA by reverse transcription-PCR in extracted RNA from islets, and release of infectious particles up to 30 days after infection without obvious cytolysis. By double IF staining, glucagon-containing a cells and insulin-containing ß cells were shown to be susceptible to CVB. The persistence of CVB3 and CVB4 in islet cells was associated with the chronic synthesis of alpha interferon (IFN-a), as evidenced by the detection of IFN-a mRNA and immunoreactive IFN-a with antiviral activity. By double IF staining, IFN-a was detected in insulin-producing ß cells only. Experiments with neutralizing anti-coxsackievirus and adenovirus receptor (CAR) antibodies provided evidence that CAR was expressed by a and ß cells and that it played a role in the infection of these cells with CVB and the consecutive IFN-a expression in ß cells. The viral replication and the expression of IFN-a in islets were not restricted to the CVB4E2 diabetogenic strain and did not depend on the genetic background of the host. The neutralization of endogenous IFN-a significantly enhanced the CVB replication in islet cells and resulted in rapid destruction of islets. Thus, human ß cells can harbor a persistent CVB infection, and CVB-induced IFN-a plays a role in the initiation and/or maintenance of chronic CVB infection in human islets.

Published
2000
Full Text
View/download PDF

69. Circulating and cell-bound antibodies increase coxsackievirus B4-induced production of IFN-alpha by peripheral blood mononuclear cells from patients with type 1 diabetes.

Author

Hober D, Chehadeh W, Weill J, Hober C, Vantyghem MC, Gronnier P, and Wattré P

Subjects
Adenoviridae immunology, Adolescent, Adult, Aged, Antibodies, Viral analysis, Cells, Cultured, Child, Child, Preschool, Diabetes Mellitus, Type 1 blood, Humans, Immunoglobulin G analysis, Immunoglobulin G pharmacology, Leukocytes, Mononuclear immunology, Middle Aged, Receptors, IgG immunology, Receptors, Virus immunology, Antibodies, Viral pharmacology, Diabetes Mellitus, Type 1 immunology, Enterovirus pathogenicity, Interferon-alpha biosynthesis, Leukocytes, Mononuclear drug effects
Abstract

Increased levels of IFN-alpha have been found in patients with type 1 diabetes who have detectable levels of coxsackievirus B4 (CVB4) RNA in their blood. The IFN-alpha-inducing activity of CVB4 in vitro is weak but can be enhanced by human IgGs. Therefore, it was investigated in vitro whether a preferential IFN-alpha response of peripheral blood mononuclear cells (PBMCs) to CVB4 exists in patients with type 1 diabetes (n=56) compared with healthy subjects (n=20) and whether antibodies play a role. In patients, the levels of IFN-alpha obtained after stimulation by PBMCs with CVB4 were higher (P=0.008), an individual IFN-alpha response by PBMCs to CVB4 was more frequent (P=0.0004) and increased levels of IFN-alpha were observed in CVB4-infected whole blood cultures. The IFN-alpha-inducing activity of patients plasma and IgGs mixed with CVB4 and then added to PBMCs was high in comparison with healthy subjects (P<0.001) and was inhibited by preincubating the cells with anti-FcgammaRII, anti-FcgammaRIII and anti-CAR (coxsackievirus and adenovirus receptor) antibodies. The strong IFN-alpha responsiveness of PBMCs to CVB4 suggested that IgGs bound to the cell surface might play a role. A short 56 degrees C incubation of PBMCs from patients responsive to CVB4 generated supernatants, which, when added to cells, exhibited IFN-alpha-enhancing activity in combination with CVB4, whereas those of controls did not. Specific antibodies for FcgammaRI, FcgammaRII and CAR inhibited this activity. These studies demonstrate that CVB4, through interactions with circulating and/or cell-bound IgGs, can strongly induce the production of IFN-alpha by PBMCs from patients with type 1 diabetes.

Published
2002
Full Text
View/download PDF

70. Human antibodies isolated from plasma by affinity chromatography increase the coxsackievirus B4-induced synthesis of interferon-alpha by human peripheral blood mononuclear cells in vitro.

Author

Chehadeh W, Bouzidi A, Alm G, Wattré P, and Hober D

Subjects
Adolescent, Adult, Antibodies, Viral isolation & purification, Child, Chromatography, Affinity, Coxsackievirus Infections blood, Female, Humans, Immune Sera pharmacology, Immunoglobulin G pharmacology, Male, Middle Aged, Antibodies, Viral pharmacology, Coxsackievirus Infections immunology, Enterovirus immunology, Interferon-alpha biosynthesis, Leukocytes, Mononuclear drug effects
Abstract

Coxsackievirus B4 (CVB4) can be found in circulating blood of patients; however, the interaction of CVB4 with peripheral blood mononuclear cells (PBMCs) is poorly understood. CVB4 induced low levels of IFN-alpha synthesis in PBMCs from healthy donors. In contrast, preincubation of infectious CVB4 with plasma from these donors containing anti-CVB4 antibodies strongly enhanced the synthesis of IFN-alpha. IgG obtained from plasma by chromatography formed immune complexes with CVB4 and increased significantly the CVB4-induced production of IFN-alpha by PBMCs. These antibodies did not have a neutralizing effect on CVB4 infection of Hep-2 cells. The role of CVB and adenovirus receptor (CAR), FcgammaRII and FcgammaRIII in the increased synthesis of IFN-alpha induced by CVB4 preincubated with IgG was shown by inhibition with specific antibodies. The major interferon-alpha-producing cells in response to CVB4-IgG complexes were CD14(+) cells and monocyte-enriched PBMCs. With the latter, detection of IFN-alpha by immunostaining was positive whereas in monocyte-depleted PBMCs it was not. This study shows that CVB4-induced synthesis of IFN-alpha by PBMCs can be enhanced by an antibody-dependent mechanism through interactions between the virus, non-neutralizing antivirus antibodies, FcgammaRII and III and CAR.

Published
2001
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results