Key result
CVB3 infection increases proapoptotic Siva expression in mouse hearts, where it interacts with muscle telethonin.
Why the study?
The mechanisms by which Coxsackievirus B3 causes acute and chronic myocarditis and dilated cardiomyopathy are not well understood.
The interaction between the proapoptotic protein Siva and telethonin may represent a molecular mechanism for cardiomyocyte damage in CVB3-induced myocarditis and dilated cardiomyopathy.
May suggest Siva-telethonin interaction in viral myocarditis; leaves open relevance to human disease and therapy.
AIMS: Coxsackievirus B3 (CVB3) is known to cause a variety of human diseases including acute and chronic myocarditis as well as dilated cardiomyopathy (DCM). However, the mechanisms by which CVB3 causes diseases are not well understood. METHODS AND RESULTS: Studies identifying protein-protein interactions during CVB3 infection are useful in delineating the pathogenesis of acute or chronic myocarditis. Screening a human heart cDNA library revealed a yet unknown interaction partner of the proapoptotic protein Siva. We demonstrate that Siva specifically interacts with the heart and skeletal muscle protein telethonin. The expression of Siva is increased in heart tissue of CVB3-infected mice and the proteins colocalize in cardiomyocytes. CONCLUSION: telethonin might be involved in CVB3-mediated cell damage and in the resulting cardiac dysfunction due to the interaction with Siva. We suggest a molecular mechanism through which coxsackieviral infection contributes to the pathogenesis of chronic myocarditis and in particular of acquired forms of DCM.
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Mihatsch et al. (2008) studied Coxsackievirus B3 (CVB3) infection. Coxsackievirus B3 (CVB3) infection was evaluated on Protein-protein interaction between Siva and telethonin. The proapoptotic protein Siva specifically interacts with the muscle protein telethonin, and its expression is increased in the heart tissue of CVB3-infected mice.
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