Connecting the Missing Link Between Dilated Cardiomyopathy and Viral Myocarditis
| Autor: | Maral Ouzounian, Peter P. Liu, M. Anne Opavsky, Yuichiro Maekawa |
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| Rok vydání: | 2007 |
| Předmět: | |
| Zdroj: | Circulation. 115:5-8 |
| ISSN: | 1524-4539 0009-7322 |
| Popis: | Myocarditis classically refers to inflammation of the heart muscle. The mechanisms include host immune dysregulation and viral triggers such as coxsackievirus (CVB), adenovirus, parvovirus, and hepatitis C virus. The pathophysiology is initiated by viral proliferation in a susceptible host, inducing host immune response. The latter, when exuberant, leads to myocyte destruction and dilated cardiomyopathy.1,2 Clinically, patients with viral myocarditis will spontaneously recover in one third of cases, persist with the disease in one third, and deteriorate in another third of the cases. Article p 94 Recent biopsy series in patients with dilated cardiomyopathy have revealed an interesting situation in which patients with symptoms of heart failure may show the presence of the viral genome alone, without any evidence of an overt inflammatory process.3 This raises the question of whether the virus can be directly responsible for the cardiomyopathy or whether it is merely an incidental bystander. Viruses are exquisitely designed nanoparticles packaged with just the critical amount of genetic material to allow them to adapt to changing host and environmental conditions and to pass on genetic material to progeny. CVBs are single-stranded RNA viruses that have natural tropism for gut epithelial cells, immune cells, neurons, and cardiomyocytes. All strains of CVBs use the coxsackie–adenoviral receptor protein to gain entry into host cells (Figure).4 The coxsackie–adenoviral receptor molecule is a critical tight-junction protein important for cell–cell communication and for maintenance of cell membrane integrity. Interestingly, viruses such as CVB must use host signaling mechanisms, including tyrosine kinases such as Abl, fyn, or p56 lck , to rearrange host actin and cytoskeleton and thus gain entry into the host cell and release viral RNA into the cytoplasm.5,6 The signaling pathways that lead from coxsackieviral (CVB) infection to the disruption of the dystrophin–sarcoglycans complex and activation of innate … |
| Databáze: | OpenAIRE |
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