Journal of IiME Volume 3 Issue 1 www.investinme.org Human enteroviruses and chronic infectious disease (continued) than ever had been suspected but that this came at a price to the virus: very slow replication and relatively very few infectious particles produced. In cases of chronic inflammatory heart disease (chronic myocarditis) or what is often thought to be a sequela of this condition, called dilated cardiomyopathy (DCM), HEV RNA has been detected in the apparent absence of cytopathic virus(4, 7, 21). We can now say with some certainty that in such cases, HEVTD populations were present. In DCM, the heart is failing due to damage to the Invest in ME (Charity Nr. 1114035) cardiomyocytes (muscle cells of the heart). Others have shown that a HEV enzyme that works on and reduces proteins, called a protease, can damage an important cardiomyocyte protein called dystrophin(3) and that in a mouse model of this disease(33), dystrophin is cleaved despite the inability of the virus to produce infectious particles and this leads to DCM in the mouse, a scenario that is closely similar to the low level production of virus particles by TD virus populations. Therefore, in this chronic HEV-induced Page 27/76
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