Muscle cell scaffold

The structural protein that anchors the heart muscle cell — and a direct target of the virus.

The Virus’s Own Scissors reduces it.

It cuts the scaffold that holds the muscle cell together — and that is a mechanical route to an enlarged heart, not an inflammatory one. 'protease 2A inhibits host cell protein synthesis, cleaves host protein dystrophin, and may induce cardiomyopathy and cardiomyocyte apoptosis' (doi 10.1007/s10495-006-0013-0 — Chau DHW et al. Coxsackievirus B3 proteases 2A and 3C induce apoptotic cell death through mitochondrial injury and cleavage of eIF4GI, Apoptosis 2007;12:513-524). It was shown directly in heart cells: 'dystrophin and eIF4G-1 ARE cleaved during coxsackievirus B3 infection of cultured myocytes' — rat neonatal ventricular cardiomyocytes, by western blot (Nat Med — Enteroviral protease 2A cleaves dystrophin: evidence of cytoskeletal disruption in an acquired cardiomyopathy). ⇒ dystrophin is the same protein whose inherited loss causes muscular dystrophy with heart failure. The virus produces an acquired version of a genetic disease. doi 10.1007/s10495-006-0013-0

It increases Heart muscle cell.

It cuts the scaffold that holds the muscle cell together — and that is a mechanical route to an enlarged heart, not an inflammatory one. 'protease 2A inhibits host cell protein synthesis, cleaves host protein dystrophin, and may induce cardiomyopathy and cardiomyocyte apoptosis' (doi 10.1007/s10495-006-0013-0 — Chau DHW et al. Coxsackievirus B3 proteases 2A and 3C induce apoptotic cell death through mitochondrial injury and cleavage of eIF4GI, Apoptosis 2007;12:513-524). It was shown directly in heart cells: 'dystrophin and eIF4G-1 ARE cleaved during coxsackievirus B3 infection of cultured myocytes' — rat neonatal ventricular cardiomyocytes, by western blot (Nat Med — Enteroviral protease 2A cleaves dystrophin: evidence of cytoskeletal disruption in an acquired cardiomyopathy). ⇒ dystrophin is the same protein whose inherited loss causes muscular dystrophy with heart failure. The virus produces an acquired version of a genetic disease. doi 10.1007/s10495-006-0013-0

It reduces Enlarged heart.

It cuts the scaffold that holds the muscle cell together — and that is a mechanical route to an enlarged heart, not an inflammatory one. 'protease 2A inhibits host cell protein synthesis, cleaves host protein dystrophin, and may induce cardiomyopathy and cardiomyocyte apoptosis' (doi 10.1007/s10495-006-0013-0 — Chau DHW et al. Coxsackievirus B3 proteases 2A and 3C induce apoptotic cell death through mitochondrial injury and cleavage of eIF4GI, Apoptosis 2007;12:513-524). It was shown directly in heart cells: 'dystrophin and eIF4G-1 ARE cleaved during coxsackievirus B3 infection of cultured myocytes' — rat neonatal ventricular cardiomyocytes, by western blot (Nat Med — Enteroviral protease 2A cleaves dystrophin: evidence of cytoskeletal disruption in an acquired cardiomyopathy). ⇒ dystrophin is the same protein whose inherited loss causes muscular dystrophy with heart failure. The virus produces an acquired version of a genetic disease. doi 10.1007/s10495-006-0013-0

It reduces Coxsackievirus B3.

And here is why the virus cuts it: the scaffold is also the cage. 'cleavage of dystrophin may have a role in release of the virus from the myocyte since vIRAL infection is increased in the absence of dystrophin' (PMID 18357777 — cvb infection and mechanisms of viral cardiomyopathy). ⇒ intact scaffold holds the virus in. Cut it, and the virus gets out to infect the next cell. the damage and the escape route are the same event. that also explains the human observation that people born without working dystrophin carry extra cardiac risk from this infection. PMID 18357777

Myocarditis Antidote (Cardiac Inflammation Resolution) →