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Research Article Free access | 10.1172/JCI109251

Viral Infection-Homograft Interactions in a Murine Model

John D. Hamilton, James F. Fitzwilliam, K. S. Cheung, John Shelburne, David J. Lang, and D. B. Amos

Medical Research Service of the Veterans Administration, Durham Veterans Administration Hospital, Durham, North Carolina 27710

Department of Medicine, Duke University, Durham, North Carolina 27710

Department of Pediatrics, Duke University, Durham, North Carolina 27710

Department of Microbiology-Immunology, Duke University, Durham, North Carolina 27710

Find articles by Hamilton, J. in: PubMed | Google Scholar

Medical Research Service of the Veterans Administration, Durham Veterans Administration Hospital, Durham, North Carolina 27710

Department of Medicine, Duke University, Durham, North Carolina 27710

Department of Pediatrics, Duke University, Durham, North Carolina 27710

Department of Microbiology-Immunology, Duke University, Durham, North Carolina 27710

Find articles by Fitzwilliam, J. in: PubMed | Google Scholar

Medical Research Service of the Veterans Administration, Durham Veterans Administration Hospital, Durham, North Carolina 27710

Department of Medicine, Duke University, Durham, North Carolina 27710

Department of Pediatrics, Duke University, Durham, North Carolina 27710

Department of Microbiology-Immunology, Duke University, Durham, North Carolina 27710

Find articles by Cheung, K. in: PubMed | Google Scholar

Medical Research Service of the Veterans Administration, Durham Veterans Administration Hospital, Durham, North Carolina 27710

Department of Medicine, Duke University, Durham, North Carolina 27710

Department of Pediatrics, Duke University, Durham, North Carolina 27710

Department of Microbiology-Immunology, Duke University, Durham, North Carolina 27710

Find articles by Shelburne, J. in: PubMed | Google Scholar

Medical Research Service of the Veterans Administration, Durham Veterans Administration Hospital, Durham, North Carolina 27710

Department of Medicine, Duke University, Durham, North Carolina 27710

Department of Pediatrics, Duke University, Durham, North Carolina 27710

Department of Microbiology-Immunology, Duke University, Durham, North Carolina 27710

Find articles by Lang, D. in: PubMed | Google Scholar

Medical Research Service of the Veterans Administration, Durham Veterans Administration Hospital, Durham, North Carolina 27710

Department of Medicine, Duke University, Durham, North Carolina 27710

Department of Pediatrics, Duke University, Durham, North Carolina 27710

Department of Microbiology-Immunology, Duke University, Durham, North Carolina 27710

Find articles by Amos, D. in: PubMed | Google Scholar

Published December 1, 1978 - More info

Published in Volume 62, Issue 6 on December 1, 1978
J Clin Invest. 1978;62(6):1303–1312. https://doi.org/10.1172/JCI109251.
© 1978 The American Society for Clinical Investigation
Published December 1, 1978 - Version history
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Abstract

The effects on some host defenses of murine cytomegalovirus (MCMV) and(or) EL4, a mouse ascites homograft, were studied in mice. Assays of cellular and humoral immunity in response to either or both of these perturbations were carried out by quantitation of various immune activities.

Limited studies demonstrated no effect of EL4 inoculation on the host response to MCMV by organ viral titer, duration of viral persistence, or anti MCMV complement-fixing antibody titer.

Prior infection with MCMV, however, resulted in greatly reduced numbers of splenocytes, the source in this study of immune effector cells. Residual splenocytes demonstrated less response to both phyto-hemagglutinin and lipopolysaccharide, particularly in the 2-3-wk interval after infection. Similarly, responder cells in mixed lymphocyte cultures were less reactive when derived from infected animals. Lymphocyte-mediated cytolysis of EL4 was significantly less in mice infected on the day of and 7, 14, and 21 days before the tumor homograft with a return to control levels by 28 days. 90% of the cell-mediated cytolysis could be eliminated by treatment with anti-theta serum. Serum-mediated cytolysis of EL4 was also reduced in infected animals. No suppressor cells or serum inhibitory factors could be identified in infected animals. Although alternative explanations exist, this study suggests that in infected animals there is a significant reduction in both the number and function of bone marrow-derived and thymus-derived cells directed against the alloantigens in EL4.

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