English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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).

Mouse Strain-related Variation as a Factor in the Pathogenesis of Coxsackievirus B3 Murine Myocarditis