Coxsackievirus B3 infection induces immune responses and metabolic remodeling that contribute to the transition from acute myocarditis to dilated cardiomyopathy and heart failure.
This review highlights the critical role of CVB3-induced immune responses and subsequent metabolic remodeling in driving the progression from acute viral myocarditis to dilated cardiomyopathy and heart failure.
Dilated cardiomyopathy (DCM) is a cardiac disease marked by the stretching and thinning of the heart muscle and impaired left ventricular contractile function. While most patients do not develop significant cardiac diseases from myocarditis, disparate immune responses can affect pathological outcomes, including DCM progression. These altered immune responses, which may be caused by genetic variance, can prolong cytotoxicity, induce direct cleavage of host protein, or encourage atypical wound healing responses that result in tissue scarring and impaired mechanical and electrical heart function. However, it is unclear which alterations within host immune profiles are crucial to dictating the outcomes of myocarditis. Coxsackievirus B3 (CVB3) is a well-studied virus that has been identified as a causal agent of myocarditis in various models, along with other viruses such as adenovirus, parvovirus B19, and SARS-CoV-2. This paper takes CVB3 as a pathogenic example to review the recent advances in understanding virus-induced immune responses and differential gene expression that regulates iron, lipid, and glucose metabolic remodeling, the severity of cardiac tissue damage, and the development of DCM and heart failure.
Yip et al. (Thu,) conducted a review in Myocarditis, Dilated Cardiomyopathy, Heart Failure. Coxsackievirus B3 (CVB3) infection was evaluated. Coxsackievirus B3 infection induces immune responses and metabolic remodeling that contribute to the transition from acute myocarditis to dilated cardiomyopathy and heart failure.