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Viral cardiomyopathy occurs when viral infections cause myocarditis with a resulting thickening of the myocardium and dilation of the ventricles. These viruses include Coxsackie B and adenovirus, echoviruses, influenza H1N1, Epstein–Barr virus, rubella (German measles virus), varicella (chickenpox virus), mumps, measles, parvoviruses, yellow fever, dengue fever, polio, rabies, and the ...
Viral-induced dilated cardiomyopathy can be characterized using different methods. A 2011 study showed in coxsackievirus infected heart proteome , increased levels of fibrotic extracellular matrix proteins and reduced amounts of energy-producing enzymes can be observed suggesting they could be characteristic in enteroviral cardiomyopathy.
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Coxsackie B is a group of six serotypes of coxsackievirus (CVB1-CVB6), a pathogenic enterovirus, that trigger illness ranging from gastrointestinal distress to full-fledged pericarditis and myocarditis (coxsackievirus-induced cardiomyopathy). [1] [2] The genome of Coxsackie B virus consists of approximately 7,400 base pairs. [3]
Myocarditis can progress to inflammatory cardiomyopathy when there are associated ventricular remodeling and cardiac dysfunction due to chronic inflammation. [ 6 ] [ 7 ] Symptoms can include shortness of breath , chest pain , decreased ability to exercise , and an irregular heartbeat . [ 1 ]
In 2015 cardiomyopathy and myocarditis affected 2.5 million people. [6] Hypertrophic cardiomyopathy affects about 1 in 500 people while dilated cardiomyopathy affects 1 in 2,500. [3] [10] They resulted in 354,000 deaths up from 294,000 in 1990. [7] [11] Arrhythmogenic right ventricular dysplasia is more common in young people. [2]
Replication follows the positive stranded RNA virus replication model. Positive stranded rna virus transcription is the method of transcription. Translation takes place by −1 ribosomal frameshifting, viral initiation, and ribosomal skipping. The virus exits the host cell by lysis, and viroporins. Human and vertebrates serve as the natural host.
Moreover, peak concentrations of T cells in the myocardium during days 7-14 play important roles in both viral clearance and immune mediated cardiac damage. T-cells not only lyse and destroy infected myocytes, but due to molecular mimicry, they also destroy normal, healthy cardiac cells, further driving the heart towards dilated cardiomyopathy.