Pathophysiological Mechanisms of Cardiac Dysfunction in Transgenic Mice with Viral Myocarditis

Viral myocarditis is pathologically associated with RNA viruses such as coxsackievirus B3 (CVB3), or more recently, with SARS-CoV-2, but despite intensive research, clinically proven treatment is limited. Here, by use of a transgenic mouse strain (TG) containing a CVB3 Delta VP0 genome we unravel virus-mediated cardiac pathophysiological processes in vivo and in vitro. Cardiac function, pathologic ECG alterations, calcium homeostasis, intracellular organization and gene expression were significantly altered in transgenic mice. A marked alteration of mitochondrial structure and gene expression indicates mitochondrial impairment potentially contributing to cardiac contractile dysfunction. An extended picture on viral myocarditis emerges that may help to develop new treatment strategies and to counter cardiac failure.

Automated summary

Using a transgenic mouse strain (TG) containing a CVB3 Delta VP0 genome, we have revealed virus-mediated cardiac pathophysiological processes in vivo and in vitro. Transgenic mice showed significant alterations in cardiac function, pathologic ECG alterations, calcium homeostasis, intracellular organization, and gene expression. The results also suggest that mitochondrial impairment may contribute to cardiac contractile dysfunction.