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Journal of General Virology (2001), 82, 1899-1907.
© 2001 Society for General Microbiology


Animal: RNA Viruses

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

Wassim Chehadeh1, Ahmed Bouzidi2, Gunar Alm3, Pierre Wattré1 and Didier Hober1

Laboratoire de Virologie, Centre Hospitalier Régional et Universitaire, Institut Gernez-Rieux, 59037 Lille Cedex, France1
SEDAC Therapeutics, IBL–CNRS, 59021 Lille, France2
Department of Veterinary Immunology, Biomedical Center, Uppsala, Sweden3

Author for correspondence: Didier Hober. Fax +33 3 20 44 52 81. e-mail dhober{at}chru-lille.fr

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), Fc{gamma}RII and Fc{gamma}RIII 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, Fc{gamma}RII and III and CAR.




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