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Two hits in viral cardiomyopathy

Enterovirus-derived C-terminal dystrophin fragment is a dominant-negative peptide representing a new therapeutic target for viral cardiomyopathy remediation. Enteroviruses infect millions each year, affecting many organ systems, including the heart. Heart-specific infections can cause dystrophic cardiomyopathy and even increase risk of death after heart attack, but the mechanisms behind these effects are unclear. Barnabei et al. found that the dystrophin cleavage product of the Coxsackievirus-encoded 2A protease was sufficient to cause severe cardiomyopathy in mice, characterized by ischemic injury, poor response to stress, and increased mortality. The C-terminal—but not N-terminal—fragment of the dystrophin cleavage product, called CtermDys, worked in a dominant-negative manner in a “two-hit” model: first localizing to the membrane of heart muscle cells, then displacing full-length dystrophin and utrophin. Giving full-length dystrophin rescued the mice from the deleterious effects of membrane-bound CtermDys, suggesting that both functional dystrophin and disruption of CtermDys are viable therapeutic approaches for enterovirus-mediated cardiomyopathy. M. S. Barnabei, F. V. Sjaastad, D. Townsend, F. B. Bedada, J. M. Metzger, Severe dystrophic cardiomyopathy caused by the enteroviral protease 2A–mediated C-terminal dystrophin cleavage fragment. Sci. Transl. Med. 7, 294ra106 (2015). [Abstract]