Nutrition has long been known to affect the ability of the host to res
pond to infectious disease. Widespread famines are often accompanied b
y increased morbidity and mortality due to infectious diseases. The cu
rrently accepted view of the relationship between nutrition of the hos
t and its susceptibility to infectious disease is one of a direct rela
tionship with host immune status. That is, if the nutritional status o
f the host is poor-due to either single or multiple nutrient deficienc
ies-then the functioning of the host immune system is compromised. Thi
s impairment of the immune response will lead to an increased suscepti
bility to infectious disease. Clearly, the immune response has been sh
own to be weakened by inadequate nutrition in many model systems and i
n human studies. However, what about the effect of host nutrition on t
he pathogen itself? Our laboratory has shown, using a mouse model of c
oxsackievirus-induced myocarditis, that a host deficiency in either se
lenium 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 phe
notype change is stable and can now be expressed even in mice of norma
l nutriture. Our results suggest that nutrition can affect not only th
e host, but the pathogen as well, and demonstrate a new model of relat
ing host nutritional effects to viral pathogenesis.