Key result
Coxsackievirus B3 infection of human monocytes stimulated dose-dependent production of TNF-alpha, IL-1 beta, and IL-6, and induced cytotoxicity against heart cells.
Population
Freshly harvested human monocytes and Girardi heart cells (in vitro model)
Comparison
Infection with coxsackievirus B3 (CVB3) vs UV-inactivated virus / uninfected baseline
Design
Preclinical
Authors
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Monocyte-derived cytokines may drive CVB3 myocarditis; hypothesis-generating for immunomodulatory targets.
CVB3 infection of human monocytes induces the production of cardiotoxic cytokines, suggesting an immunologic mechanism for cardiac damage in viral myocarditis.
Henke et al. (1992) studied Myocarditis. Coxsackievirus B3 (CVB3) vs. UV-inactivated virus was evaluated on Cytokine release (TNF-alpha, IL-1 beta, IL-6) and gene expression. Coxsackievirus B3 infection of human monocytes stimulated dose-dependent production of TNF-alpha, IL-1 beta, and IL-6, and induced cytotoxicity against heart cells.
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