A sometimes fatal heart enlargement can be inherited or acquired through infection. In this month's issue of Nature Medicine , the scientists show that the virus causes symptoms in the same way as genes are faulty, suggesting that a single therapy could work against the disease.
Dilated cardiomyopathy, which can cause shortness of breath and the result of heart failure and death, affects about 50,000 people in the United States each year. For several years, researchers know that up to a third of patients suffering from viral infections, most of them with the Coxsackie B virus infections swell and irritates the heart, sometimes leading to chronic inflammation which can lead to cardiomyopathy. Cardiomyopathy but can also be caused by genetic diseases such as muscular dystrophy, which causes abnormalities in a protein called dystrophin. Dystrophin is responsible for binding of the cell membrane to contractile proteins such as actin and allows the force of contraction in the cells to be transmitted outside.
Cardiologist Kirk Knowlton San Diego University and his colleagues wanted to know if the Coxsackie B virus also affected dystrophin. The researchers showed that in test tubes, proteins produced by the virus Coxsackie B virus separated dystrophin, but not to other proteins present in cardiac cells. After the rat heart cells in culture were infected with Coxsackie virus B virus, the amount of normal dystrophin decreased within 3 days. Finally, the researchers injected immunodeficient mice with Coxsackie B virus when they killed animals a week later, they found that the virus had broken dystrophin in their hearts and that the membranes of heart cells infected with Coxsackie virus B were more permeable to blue dye than uninfected cells. This implies that the distribution of dystrophin damaged cell membranes, said Knowlton; this weakening of cell membranes allows the virus to spread, but damages the heart, as it makes the cells less resistant and less able to contract effectively. In an attempt to keep pumping enough blood, the heart starts getting larger.
The study is the first to show that the damaged dystrophin underlies both genetic and acquired cardiomyopathy, said Jeffrey A. Towbin, a cardiologist with the Baylor College of Medicine and Children's Hospital of Texas in Houston. This similarity suggests that researchers should target the underlying process in different varieties of the disease, he says, for example by developing a drug to prevent the dystrophin breaking down.
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