Key result
Cardiotropic viruses are important pathogenic factors in dilated cardiomyopathy, offering new therapeutic targets in virus uptake, innate immune signaling, and viral gene silencing.
This review outlines novel molecular targets for treating chronic viral cardiomyopathy, emphasizing the potential of targeting virus uptake, innate immune signaling, and viral proteins.
May inform antiviral strategies in dilated cardiomyopathy; hypothesis-generating pending prospective trials.
Dilated cardiomyopathy (DCM) is a prevalent heart muscle disease characterized by impaired contractility and dilation of the ventricles. Recent clinical research suggests that cardiotropic viruses are important environmental pathogenic factors in human DCM, which may therefore be considered as a chronic viral cardiomyopathy. All virus-positive DCM patients thus come into the focus of virological research and should be considered for antiviral strategies. Interferon-beta therapy has been shown to mediate virus elimination in patients with adenovirus or coxsackievirus persistence. We discuss here several possible new molecular targets for patients infected with cardiotropic viruses in (1) the cellular virus uptake system, (2) virus-induced cellular signaling pathways, and (3) interactions between virus-encoded proteins with important cellular target proteins. The potential of these approaches in the setting of a chronic viral infection is significantly different from that in an acute viral infection. Specific problems encountered in a chronic situation and possible solutions are discussed.
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Poller et al. (2006) conducted a review in Chronic Viral Cardiomyopathy / Dilated Cardiomyopathy (n=245). Antiviral strategies (receptor blockade, innate immunity modulation, RNA interference) was evaluated. Cardiotropic viruses are important pathogenic factors in dilated cardiomyopathy, offering new therapeutic targets in virus uptake, innate immune signaling, and viral gene silencing.
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