Variations in the susceptibility to coxsackievirus B3-induced myocarditis among different strains of mice

L. J. Wolfgram, Kirk Beisel, A. Herskowitz, N. R. Rose

Research output: Contribution to journalArticle

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Abstract

This study was undertaken to examine the inherent predisposition of different inbred strains of mice to develop Coxsackievirus B3-induced myocarditis. A time course study established the pertinent, differential parameters of the disease and their corresponding genetic control. The A.BY/SnJ (H-2b), A.SW/SnJ (H-2(s)), A.CA/SnJ (H-2(f)), B10.S/SgSf (H-2(s)), B10.PL/SgSf (H-2(u)), and C3H.NB/SnJ (H-2(p)) strains were found to vary widely in the extent and duration of viremia, in the temporal appearance and titer of neutralizing antibody, and in the prevalence, severity, and duration of mycoardial disease. The A.BY/SnJ (H-2b), A.SW/SnJ (H-2(s)), A.CA/SnJ (H-2(f)), and C3H.NB/SnJ (H-2(p)) mice developed continuing, chronic myocardial disease, whereas B10.S/SgSf (H-2(s)) and B10.PL/SgSf (H-2(u)) did not. The four strains that displayed prolonged myocarditis also produced heart-specific myocardial autoantibodies. Heart-specific autoantibodies were not found in the B10.S/SgSf and B10.PL/SgSf animals. Differences in prevalence and titer of these heart-specific autoantibodies were noted among the three A strain H-2 congenic lines. The influence of the major histocompatibility complex (MHC) on disease production was demonstrated by comparison of the three A strain and two B10 strain H-2 congenics. Differences between A.SW/SnJ (H-2(s)) and B10.S/SgSf (H-2(s)) suggested non-MHC control of disease. These studies additionally indicate that the genetic regulation of susceptibility to CB3 infection and the direct virus-induced inflammation differ from the later immunopathic myocarditis.

Original languageEnglish
Pages (from-to)1846-1852
Number of pages7
JournalJournal of Immunology
Volume136
Issue number5
StatePublished - 1986
Externally publishedYes

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Enterovirus
Myocarditis
Autoantibodies
Major Histocompatibility Complex
Inbred Strains Mice
Viremia
Virus Diseases
Genetic Predisposition to Disease
Neutralizing Antibodies
Cardiomyopathies
Chronic Disease
Inflammation

All Science Journal Classification (ASJC) codes

  • Immunology

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Variations in the susceptibility to coxsackievirus B3-induced myocarditis among different strains of mice. / Wolfgram, L. J.; Beisel, Kirk; Herskowitz, A.; Rose, N. R.

In: Journal of Immunology, Vol. 136, No. 5, 1986, p. 1846-1852.

Research output: Contribution to journalArticle

Wolfgram, L. J. ; Beisel, Kirk ; Herskowitz, A. ; Rose, N. R. / Variations in the susceptibility to coxsackievirus B3-induced myocarditis among different strains of mice. In: Journal of Immunology. 1986 ; Vol. 136, No. 5. pp. 1846-1852.
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abstract = "This study was undertaken to examine the inherent predisposition of different inbred strains of mice to develop Coxsackievirus B3-induced myocarditis. A time course study established the pertinent, differential parameters of the disease and their corresponding genetic control. The A.BY/SnJ (H-2b), A.SW/SnJ (H-2(s)), A.CA/SnJ (H-2(f)), B10.S/SgSf (H-2(s)), B10.PL/SgSf (H-2(u)), and C3H.NB/SnJ (H-2(p)) strains were found to vary widely in the extent and duration of viremia, in the temporal appearance and titer of neutralizing antibody, and in the prevalence, severity, and duration of mycoardial disease. The A.BY/SnJ (H-2b), A.SW/SnJ (H-2(s)), A.CA/SnJ (H-2(f)), and C3H.NB/SnJ (H-2(p)) mice developed continuing, chronic myocardial disease, whereas B10.S/SgSf (H-2(s)) and B10.PL/SgSf (H-2(u)) did not. The four strains that displayed prolonged myocarditis also produced heart-specific myocardial autoantibodies. Heart-specific autoantibodies were not found in the B10.S/SgSf and B10.PL/SgSf animals. Differences in prevalence and titer of these heart-specific autoantibodies were noted among the three A strain H-2 congenic lines. The influence of the major histocompatibility complex (MHC) on disease production was demonstrated by comparison of the three A strain and two B10 strain H-2 congenics. Differences between A.SW/SnJ (H-2(s)) and B10.S/SgSf (H-2(s)) suggested non-MHC control of disease. These studies additionally indicate that the genetic regulation of susceptibility to CB3 infection and the direct virus-induced inflammation differ from the later immunopathic myocarditis.",
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AB - This study was undertaken to examine the inherent predisposition of different inbred strains of mice to develop Coxsackievirus B3-induced myocarditis. A time course study established the pertinent, differential parameters of the disease and their corresponding genetic control. The A.BY/SnJ (H-2b), A.SW/SnJ (H-2(s)), A.CA/SnJ (H-2(f)), B10.S/SgSf (H-2(s)), B10.PL/SgSf (H-2(u)), and C3H.NB/SnJ (H-2(p)) strains were found to vary widely in the extent and duration of viremia, in the temporal appearance and titer of neutralizing antibody, and in the prevalence, severity, and duration of mycoardial disease. The A.BY/SnJ (H-2b), A.SW/SnJ (H-2(s)), A.CA/SnJ (H-2(f)), and C3H.NB/SnJ (H-2(p)) mice developed continuing, chronic myocardial disease, whereas B10.S/SgSf (H-2(s)) and B10.PL/SgSf (H-2(u)) did not. The four strains that displayed prolonged myocarditis also produced heart-specific myocardial autoantibodies. Heart-specific autoantibodies were not found in the B10.S/SgSf and B10.PL/SgSf animals. Differences in prevalence and titer of these heart-specific autoantibodies were noted among the three A strain H-2 congenic lines. The influence of the major histocompatibility complex (MHC) on disease production was demonstrated by comparison of the three A strain and two B10 strain H-2 congenics. Differences between A.SW/SnJ (H-2(s)) and B10.S/SgSf (H-2(s)) suggested non-MHC control of disease. These studies additionally indicate that the genetic regulation of susceptibility to CB3 infection and the direct virus-induced inflammation differ from the later immunopathic myocarditis.

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