Key result
Transgenic expression of the HCV-core protein in mice induced cardiomyopathy characterized by ventricular dilatation and dysfunction after 12 months of age.
Why the study?
Does the HCV-core protein induce cardiomyopathy in a transgenic mouse model?
Does the HCV-core protein induce cardiomyopathy in a transgenic mouse model?
The HCV-core protein directly induces cardiomyopathy in a transgenic mouse model, providing a mechanistic link between chronic HCV infection and heart failure.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in mice; leaves open whether HCV-core contributes to human cardiomyopathy.
Hepatitis C virus (HCV) has been reported to be associated with cardiomyopathy. However, the mechanism of cardiomyopathy in chronic HCV infection is still unclear. Therefore, we investigate the development of cardiomyopathy in mice transgenic for the HCV-core gene. After the age of 12 months, mice developed cardiomyopathy that appeared as left ventricular dilatation, and systolic and diastolic dysfunction assessed by Doppler echocardiography. Histologically, hypertrophy of cardiomyocytes, cardiac fibrosis, disarray and scarcity of myofibrils, vacuolization and deformity of nuclei, myofibrillar lysis, streaming of Z-bands, and an increased number of bizarre-shaped mitochondria were found in HCV-core transgenic mice. These histological changes are just consistent with cardiomyopathy. In conclusion, the HCV-core protein directly plays an important role in the development of cardiomyopathy.
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Omura et al. (2004) studied Cardiomyopathy. HCV-core gene expression was evaluated on Development of cardiomyopathy (left ventricular dilatation, systolic and diastolic dysfunction, and histological changes). Transgenic expression of the HCV-core protein in mice induced cardiomyopathy characterized by ventricular dilatation and dysfunction after 12 months of age.
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