The Induction of Gross Myocardial Lesions by a Coxsackie (Pleurodynia) Virus and Cortisone 12

Kilbourne, Edwin D.; Wilson, Charles B.; Perrier, Dorothy

doi:10.1172/jci103286

Cited by 125 publications

(33 citation statements)

References 8 publications

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“…For example, the efficacy of immunosuppressive therapy for viral myocarditis has been controversial, based upon both clinical8 9 and experimental studies. [10][11][12][13] Recently, monoclonal antibody therapy has been explored in some diseases, focusing upon the etiologic factors. [14][15][16] Coxsackievirus B has been established as the predominant cause of viral myocarditis in humans.…”

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confidence: 99%

Monoclonal antibody therapy for prevention of acute coxsackievirus B3 myocarditis in mice.

Kishimoto¹,

Abelmann²

1989

Circulation

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The efficacy of monoclonal antibodies against T cell subsets in the therapy of experimental myocarditis caused by coxsackievirus B3 (CB3) was investigated. Two-week-old male C3H/He mice were inoculated with CB3 virus. Treatment was begun in the viremic stage (starting on the day of inoculation) in experiment 1 and in the later aviremic stage (starting on day 10) in experiment 2. Rat anti-mouse monoclonal antibodies, Lyt 1 (helper/inducer T) at 1 microgram/mouse (group 2 in experiment 1; group 6 in experiment 2), Lyt 2 (suppressor/cytotoxic T) at 1 microgram/mouse (group 3 in experiment 1; group 7 in experiment 2), and Lyt 1 at 1 microgram plus Lyt 2 at 1 microgram/mouse (group 4 in experiment 1; group 8 in experiment 2), were administered subcutaneously daily for 2 weeks. The treatment groups were compared with infected controls (group 1 in experiment 1; group 5 in experiment 2). In experiment 1, the survival rate in group 4 was higher (p less than 0.01) than in group 1. In experiment 2, mice treated with Lyt 1 plus Lyt 2 (group 8) survived significantly longer (p less than 0.05) than did controls (group 5). In experiment 1, myocardial virus titers on days 5 and 6 did not show any significant differences among the four groups. Serum-neutralizing antibody titers between group 1 and group 4 in experiment 1 or between group 5 and group 8 in experiment 2 did not differ significantly. Histologic examination showed extensive myocardial necrosis and cellular infiltration in untreated groups: there was less infiltration in group 4 and in group 8 and less severe necrosis in group 8.(ABSTRACT TRUNCATED AT 250 WORDS)

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confidence: 99%

Monoclonal antibody therapy for prevention of acute coxsackievirus B3 myocarditis in mice.

Kishimoto¹,

Abelmann²

1989

Circulation

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“…Treatment of viral myocarditis in humans by steroids and nonsteroid immunosuppressive agents is highly controversial (19), the results often being based on poorly controlled and frequently anecdotal observations. Studies in CVB murine models of myocarditis show that cortisone and immunosuppressive agents markedly exacerbate the extent of myocarditis and increase the rate of mortality among the recipients (3,11,12,28). Also, levamisole, an immunopotentiating agent, markedly exacerbates CVB3-induced myocarditis (5).…”

Section: Resultsmentioning

confidence: 99%

“…Introduction of these viruses by natural routes (inhalation or ingestion) (10,22) or parenteral routes (38) produces heart disease with minimal to no symptoms in 90% or more of mice. Virus replication takes place in many organs; however, replication in heart cells induces formation of a myocardial lesion: focal eosinophilic degeneration of cells with infiltration of mononuclear and polymorphonuclear cells (4,12,34,40).…”

mentioning

confidence: 99%

Antimyocarditic activity of the guanine derivative BIOLF-70 in a coxsackievirus B3 murine model

Gauntt¹,

Arizpe²,

Kung³

et al. 1985

Antimicrob Agents Chemother

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Prophylactic administration of a nontoxic dose of 9- [[2-benzyloxyl-l-(benzyloxymethyl)ethoxy]methyl]-6-chloroguanine (BIOLF-70) to mice reduced the number of myocarditic lesions induced by coxsackievirus B3 (CVB3). BIOLF-70 exhibited minimal antiviral activity against CVB3 in HeLa cells and murine neonatal skin fibroblasts and mininally reduced CVB3 yields in heart tissues. The drug had no effect on serum anti-CVB3 neutralizing antibody titers and did not induce the production of interferon. Flow microfluorometric analyses of splenic lymphocytes taken from BIOLF-70-treated, CVB3-inoculated mice at 7 days postinoculation showed that the proportion of T lymphocytes was increased, as measured by fluorescent staining of Thy-1 and Lyt-2 surface markers, compared with the proportion of T lymphocytes in splenic cells from virus-inoculated or BIOLF-70-treated or normal groups of mice. Splenic lymphocytes from BIOLF-70-treated, CVB3-inoculated mice showed reduced cytotoxic activity against CVB3-infected target fibroblasts. Splenic cells from BIOLF-70-treated, CVB3-inoculated mice had slightly higher natural killer cell activity than did those from the other three groups of mice, which had comparatively similar levels of natural killer cell activity. The data suggest that BIOLF-70 exerts antimyocarditic activity perhaps by some antiviral activity in heart tissues and by immunomodulatory mechanisms which appear to involve T suppressor or T cytotoxic lymphocyte subpopulations and natural killer cells.

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“…Coxsackievirus B3 infection, which is tolerated in normal adult mice (1), produces servere disease in mice subjected to sustained post-weaning undernutrition (marasmus) (2). Marasmic mice show persistence of infective virus in the heart, spleen, liver, and pancreas, and an increased occurrence of massive hepatic necrosis, gross cardiac lesions, and death.…”

mentioning

confidence: 99%

“…These animals can be significantly protected from the severe sequellae of viral infection by the institution of an optimal diet at the time of viral challenge. Complete protection is achieved if the animals are fed an optimal diet for about 1 month before viral infection (2).…”

mentioning

confidence: 99%

Modification of Severe Coxsackievirus B ₃ Infection in Marasmic Mice by Transfer of Immune Lymphoid Cells

Woodruff

1971

Proc. Natl. Acad. Sci. U.S.A.

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The Induction of Gross Myocardial Lesions by a Coxsackie (Pleurodynia) Virus and Cortisone 12

Cited by 125 publications

References 8 publications

Monoclonal antibody therapy for prevention of acute coxsackievirus B3 myocarditis in mice.

Monoclonal antibody therapy for prevention of acute coxsackievirus B3 myocarditis in mice.

Antimyocarditic activity of the guanine derivative BIOLF-70 in a coxsackievirus B3 murine model

Modification of Severe Coxsackievirus B ₃ Infection in Marasmic Mice by Transfer of Immune Lymphoid Cells

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The Induction of Gross Myocardial Lesions by a Coxsackie (Pleurodynia) Virus and Cortisone 12

Cited by 125 publications

References 8 publications

Monoclonal antibody therapy for prevention of acute coxsackievirus B3 myocarditis in mice.

Monoclonal antibody therapy for prevention of acute coxsackievirus B3 myocarditis in mice.

Antimyocarditic activity of the guanine derivative BIOLF-70 in a coxsackievirus B3 murine model

Modification of Severe Coxsackievirus B 3 Infection in Marasmic Mice by Transfer of Immune Lymphoid Cells

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Modification of Severe Coxsackievirus B ₃ Infection in Marasmic Mice by Transfer of Immune Lymphoid Cells