Summary
Coxsackie B viruses are a common cause of viral myocarditis in humans. A murine model of the human disease has been developed using Coxsackievirus group B, type 3 and inbred Balb/c mice. Infection of T lymphocyte deficient mice does not result in significant myocarditis indicating the importance of T cells in this disease. The virus can be isolated from the hearts of T cell deficient and normal mice in equal concentrations. Virus elimination presumably is mediated by virus specific neutralizing antibody induced in both groups. T lymphocytes, natural killer cells and macrophage obtained from normal virus infected mice are all capable of lysing myofibers in vitro. Maximum lysis is obtained with the cytolytic T cells. When these cell populations or Coxsackievirus immune antibody were adoptively transferred into T lymphocyte deficient animals infected with the virus, only animals given T cells developed significant myocarditis.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
Similar content being viewed by others
References
Bollon, A.P., Nath, K. and Shay, J.W. Establishment of contracting heart muscle cell culture. Tissue Culture Association Manual 3, 637–640 (1977)
Cantor, H. and Boyse E.A. Functional subclasses of T lymphocytes bearing different Ly antigens.I. The generation of functionally distinct T-cell subclasses is a differentiation process independent of antigen. Journal Experimental Medicine 141, 1376–1399 (1975)
Crowell, R.L. and Syverton, J.T. The mammalian cell-virus relationship. VI Sustained infection of HeLa cells by Coxsackie B-3 virus and effect on superinfection. Journal Experimental Medicine 113, 419–435 (1961)
Doherty, P.C., Blanden, R.V. and Zinkernagel, R.M. Specificity of virus-immune effector T cells for H-2K or H-2D compatible interactions: Implications for H-antigen diversity. Transplantation Review 29, 89–124 (1976)
Evans, R. and Alexander, P. Mechanisms of immunologically specific killing of tumor cells by macrophages. Nature 236, 168–170 (1972)
Fidler, I.J. Activation in vitro of mouse macrophages by syngeneic, allogeneic or xenogeneic lymphocyte supernatants. Journal of National Cancer Institute 55, 1159–1163 (1975)
Godman, G.C. The cytopathology of enteroviral infection. International Review of Experimental Pathology 5, 67–110 (1966)
Herberman, R.B., Nunn, M.F. and Lavren, D.H. Natural cytotoxic reactivity of mouse lymphoid cells against syngeneic and allogeneic tumor. II Characterization of effector cells. International Journal Cancer 16, 230–239 (1975)
Huber, S.A., Job, L.P. and Woodruff, J.F. Lysis of infected myofibers by Coxsackievirus B-3-immune T lymphocytes. American Journal of Pathology 98, 681–694 (1980)
Huber, S.A., Job, L.P. and Woodruff, J.F. Sex-related differences in the pattern of Coxsackievirus B-3-induced immune spleen cell cytotoxicity against virus infected myofibers. Infection and Immunity 32, 68–73 (1981)
Huber, S.A., Job, L.P., Auld, K.R. and Woodruff, J.F. Sex-related differences in the rapid production of cytotoxic spleen cells active against uninfected myofibers during Coxsackievirus B-3 infection. Journal of Immunology 126, 1336–1340 (1981)
Huber, S.A., Job, L.P. and Auld, K.R. Influence of sex hormones on Coxsackie B-3 virus infection in Balb/c mice. Cellular Immunology 67, 173–189 (1982)
Kim, Y-B., Huk, N.D., Koren, H.S. and Amos, D.B. Natural killing (NK) and antibody-dependent cellular cytotoxicity (ADCC) in specific pathogen-free (SPF) miniature swine and germ-free piglets. I comparison of NK and ADCC. Journal of Immunology 125, 755–762 (1980).
Kisielow, P., Hirst, J.A., Shiku, M., Beverley, P.C.L., Boyse, E.A. and Oettegen, H.F. Ly antigens as markers for functionally distinct subpopulations of thymus-derived lymphocytes of the mouse. Nature 253, 219–220 (1975)
Lerner, A.M. and Wilson, F.M. Virus myocaridopathy. Progress in Medical Virology 15, 63–91 (1973)
Oberg, B and Phillipson, L. Replication of Poliovirus RNA studied by gel filtration and electrophoresis. European Journal Biochemistry 11, 305–315 (1969)
Oldstone, M.B.A. Virus neutralization and virus-induced immune complex disease. Progress in Medical Virology 19, 84–119 (1975)
Rager-Zisman, B. and Allison, A.C. The role of antibody and host cells in the resistance of mice against infection with Coxsackie B-3 virus. Journal of General Virology 19, 329–338 (1973)
Rager-Zisman, B. and Allison, A.C. Effects of immunosuppression on Coxsackie B-3 virus infection in mice, and passive protection by circulating antibody. Journal of General Virology 19, 339–351 (1973)
Ruddle, N.H. Delayed hypersensitivity to soluble antigens in mice II analysis in vitro. International Archives Allergy Applied Immunology 58, 44–52 (1979)
Welsh, R.M. Cytotoxic cells induced during lymphocytic choriomeningitis virus infection of mice. I.Characterization of natural killer cell induction. Journal of Experimental Medicine 148, 163–181 (1978)
Woodruff, J.F. Lack of correlation between neutralizing antibody production and suppression of Coxsackievirus B-3 replication in target organs: Evidence for involvement of mononuclear inflammatory cells in host defense. Journal of Immunology 123, 31–36 (1979)
Woodruff, J.F. Viral myocarditis. American Journal of Pathology 101, 425–484 (1980)
Woodruff, J.F. and Woodruff, J.J. Involvement of T lymphocytes in the pathogenesis of Coxsackie virus B-3 heart disease. Journal of Immunology 113, 1726–1734 (1974)
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1983 Plenum Press, New York
About this chapter
Cite this chapter
Huber, S.A., Job, L.P. (1983). Cellular Immune Mechanisms in Coxsackievirus Group B, Type 3 Induced Myocarditis in Balb/C Mice. In: Spitzer, J.J. (eds) Myocardial Injury. Advances in Experimental Medicine and Biology, vol 161. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4472-8_29
Download citation
DOI: https://doi.org/10.1007/978-1-4684-4472-8_29
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4684-4474-2
Online ISBN: 978-1-4684-4472-8
eBook Packages: Springer Book Archive