Mouse Strain-related Variation as a Factor in the Pathogenesis of Coxsackievirus B3 Murine Myocarditis
Khatib, Riad and Probert, Albert and Reyes, Milagros P. and Khatib, Ghada and Chason, Jacob L.,, 68, 2981-2988 (1987),
doi = https://doi.org/10.1099/0022-1317-68-12-2981,
publicationName = Microbiology Society,
issn = 0022-1317,
abstract= 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).,
language=,
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