Mechanisms of Immunosuppression in Cytomegalovirus Mononucleosis. II. Virus-Monocyte Interactions

Virus-monocyte interactions wereevaluated in patients with mononucleosis due to cytomegalovirus (CMV). Group 1patients studied about two weeks after the onset of symptoms had lymphocyte responses to concanavalin A (con A) that were maximally suppressed and unaffected by in vitro culture or reconstit...

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Published inThe Journal of infectious diseases Vol. 144; no. 1; pp. 47 - 54
Main Authors Carney, Walter P., Hirsch, Martin S.
Format Journal Article
LanguageEnglish
Published United States The University of Chicago Press 01.07.1981
University of Chicago Press
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Summary:Virus-monocyte interactions wereevaluated in patients with mononucleosis due to cytomegalovirus (CMV). Group 1patients studied about two weeks after the onset of symptoms had lymphocyte responses to concanavalin A (con A) that were maximally suppressed and unaffected by in vitro culture or reconstitution with monocytes. Lymphocytes from group 2 patients studied about three weeks after the onset of symptoms had less markedly suppressed responses, which were reversed by in vitro culture or by reconstitution with monocytes. Monocytedepletion resulted in a marked diminution of fresh lymphocyte responses of group 2 patients but not of group 1 patients. CMV was isolated from blood monocytes of four patients with mononucleosis; intact, infected monocytes were capable of suppressing responses of cultured autologous lymphocytes to con A. Monocytes from uninfected control donors were infected in vitro with CMV and evaluated for the induction of suppressor activity. CMV-infected monocytes were significantly more suppressive for autologous lymphocyteresponses to con A than were uninfected monocytes.
Bibliography:ark:/67375/HXZ-SVXHQKD7-B
istex:B35617C8F3A545DB9BBEFC5098B82CDE54ED4A26
Please address requests for reprints to Dr. Walter P. Carney, Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114.
ObjectType-Article-2
SourceType-Scholarly Journals-1
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ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/144.1.47