HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Selgrade, M. K. Articles by Steinberg, A. D. Search for Related Content PubMed Articles by Selgrade, M. K. Articles by Steinberg, A. D.

Effect of Murine Cytomegalovirus on the in Vitro Responses of T and B Cells to Mitogens¹

From the Clinical and Experimental Immunology Department, Cellular Immunology Division, Naval Medical Research Institute, and the Arthritis and Rheumatism Branch, National Institute of Arthritis, Metabolism and Digestive Diseases, National Institutes of Health, Bethesda, Maryland 20014

Abstract

Both in vitro and in vivo murine cytomegalovirus (MCMV) infection depressed the responses of lymphocytes to both B and T cell mitogens. The possibilities that macrophages or nonspecific T cell inhibition of B cells might account for the depressed responses were eliminated. In vitro data suggested that B cell responses are more susceptible to this depression than T cell responses. The possibility that the depression of T cell responses is not a direct effect of viral infection of lymphocytes is discussed.

To investigate further the interaction between B and T lymphocytes and MCMV, mice with B and T cell deficiences were studied. A comparison of the susceptibility of athymic Nu/Nu mice and T cell competent Nu/+ littermates to MCMV showed that the LD₅₀ for Nu/Nu mice is 10-fold lower than that for Nu/+ mice, but Nu/+ mice given an LD₅₀ of virus died much sooner after infection than Nu/Nu mice given an LD₅₀. Pathogenic mechanisms responsible for death may be different in these two groups of mice. Similarly the MCMV LD₅₀ for B cell-deficient mice (treated with goat anti-mouse IgM serum) was 10-fold lower than the LD₅₀ for mice treated with normal goat serum, but given an LD₅₀ of virus, the latter died sooner after infection than the former. In contrast, there was little difference between the LD₅₀ or time of death after MCMV infection of CBA x DBA F₁ male mice (which are deficient in their response to thymic independent antigens) and their normal littermates, the CBA x DBA F₁ female mice.

Footnotes

¹ This work was supported by the Naval Medical Research and Development Command Work Unit No. MF51.524.013.1004AB2C. The opinions or assertions contained herein are the private ones of the authors and are not to be construed as official or reflecting the views of the United States Navy Department or the naval service at large. The animals used in this study were handled in accordance with the provisions of Public Law 89-54 as amended by Public Law 91-579, "Animal Welfare Act of 1970," and the principles outlined in the "Guide for the Care of Laboratory Animals," United States Department of Health, Education, and Welfare Publication No. (NIH) 73-23.

² Present address: Department of Bacteriology, University of North Carolina, Chapel Hill, North Carolina 27514.

³ To whom reprint requests should be addressed at Clinical and Experimental Immunology Department, Cellular Immunology Division, Naval Medical Research Institute, Bethesda, Maryland 20014.

⁴ Present address: Department of Internal Medicine, University of California at Davis, School of Medicine, Davis, California 95616.