摘要
Keshan disease, an endemic cardiomyopathy in China, can be prevented with selenium (Se) supplementation. However, the seasonal and annual nature of the disease suggests that an infectious co-factor is required along with a deficiency in Se. Using a murine model of coxsackievirus B3 (CVB3) -induced myocarditis, Se-deficient mice were shown to be more susceptible to the cardiopathologic effects of the virus. In addition, a normall benign strain of CVB3 becomes virulent in Se-deficient mice. This change in virulence was shown to be due to point mutations in the viral genorne. Although the mechanism of the viral mutation is not known, the oxidative stress status of the Se-deficient host may play a role, either by directly affecting the virus and/or affecting host immune defenses
Keshan disease, an endemic cardiomyopathy in China, can be prevented with selenium (Se) supplementation. However, the seasonal and annual nature of the disease suggests that an infectious co-factor is required along with a deficiency in Se. Using a murine model of coxsackievirus B3 (CVB3) -induced myocarditis, Se-deficient mice were shown to be more susceptible to the cardiopathologic effects of the virus. In addition, a normall benign strain of CVB3 becomes virulent in Se-deficient mice. This change in virulence was shown to be due to point mutations in the viral genorne. Although the mechanism of the viral mutation is not known, the oxidative stress status of the Se-deficient host may play a role, either by directly affecting the virus and/or affecting host immune defenses.
