Rapid genomic evolution of a non-virulent coxsackievirus B3 in selenium-deficient mice.
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 normal 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 genome. 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.
Beck
M A
MA
University of North Carolina at Chapel Hill, Frank Porter Graham Child Development Center 27599-8180, USA.
D000818:Animals; D005075:Biological Evolution; D003384:Coxsackievirus Infections / Q000150:complications / Q000276:immunology; D003677:Deficiency Diseases / Q000150:complications / Q000276:immunology / Q000821:virology*; D004195:Disease Models, Animal; D029822:Enterovirus B, Human / Q000235:genetics* / Q000472:pathogenicity; D016679:Genome, Viral; D051379:Mice; D009205:Myocarditis / Q000150:complications / Q000821:virology; D017354:Point Mutation; D012643:Selenium / Q000172:deficiency*
D012643:Selenium