Increased virulence of coxsackievirus B3 in mice due to vitamin E or selenium deficiency.

Nutrition has long been known to affect the ability of the host to respond to infectious disease. Widespread famines are often accompanied by increased morbidity and mortality due to infectious diseases. The currently accepted view of the relationship between nutrition of the host and its susceptibility to infectious disease is one of a direct relationship with host immune status. That is, if the nutritional status of the host is poor-due to either single or multiple nutrient deficiencies-then the functioning of the host immune system is compromised. This impairment of the immune response will lead to an increased susceptibility to infectious disease. Clearly, the immune response has been shown to be weakened by inadequate nutrition in many model systems and in human studies. However, what about the effect of host nutrition on the pathogen itself? Our laboratory has shown, using a mouse model of coxsackievirus-induced myocarditis, that a host deficiency in either selenium or vitamin E leads to a change in viral phenotype, such that an avirulent strain of the virus becomes virulent and a virulent strain becomes more virulent. The change in phenotype was shown to be due to point mutations in the viral genome. Once the mutations occur, the phenotype change is stable and can now be expressed even in mice of normal nutriture. Our results suggest that nutrition can affect not only the host, but the pathogen as well, and demonstrate a new model of relating host nutritional effects to viral pathogenesis.