Key result
The pathogenesis of myocardial fiber destruction during the acute phase of Coxsackievirus B3 murine myocarditis remains uncertain, though immune mechanisms involving cytotoxic T lymphocytes are proposed.
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Clinical management of viral myocarditis unchanged; leaves open cytotoxic T lymphocyte role in murine models.
Coxsackievirus B3 (CB3) is a well known cause of acute heart muscle disease in humans and experimental animals. After virus is cleared from the heart, a subacute myocarditis or cardiomyopathy may ensue and these conditions are thought to be due to host immune response. During the acute phase of myocarditis, however, the pathogenesis of myocardial fibre destruction remains uncertain. One theory proposing an immune mechanism is based on the 2 to 3 day delay in pathological changes observed after peak virus titres in the heart and their chronological synchrony with the development of cytotoxic T lymphocyte (CTL) activity in the spleen of infected animals (Khatib et al., 1980; Woodruff & Woodruff, 1974). Moreover, adoptively transferred, Cr-labelled sensitized T cells are re-routed to the heart at about the time when myocardial fibre damage becomes apparent by light microscopy (Reyes et al., 1984).
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Khatib et al. (1987) conducted a review in Coxsackievirus B3 Murine Myocarditis. Coxsackievirus B3 infection was evaluated. The pathogenesis of myocardial fiber destruction during the acute phase of Coxsackievirus B3 murine myocarditis remains uncertain, though immune mechanisms involving cytotoxic T lymphocytes are proposed.
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