Department of Pediatrics, University of North Carolina at Chapel Hill,
Chapel Hill, NC 27599, USA. melinda_beck@unc.edu
The discovery that the juvenile cardiomyopathy known as Keshan disease
likely has a dual etiology that involves both a nutritional deficiency of
the essential trace mineral selenium (Se) as well as an infection with an
enterovirus provided the impetus for additional studies of relationships
between nutrition and viral infection. An amyocarditic strain of
coxsackievirus B3, CVB3/0, converted to virulence when it was inoculated
into Se-deficient mice. This conversion was accompanied by changes in the
genetic structure of the virus so that its genome closely resembled that
of other known virulent CVB3 strains. Similar alterations in virulence and
genomic composition of CVB3/0 could be observed in mice fed normal diets
but genetically deprived of the antioxidant selenoenzyme glutathione
peroxidase (knockout mice). More recent research has shown that a mild
strain of influenza virus, influenza A/Bangkok/1/79, also exhibits
increased virulence when given to Se-deficient mice. This increased
virulence is accompanied by multiple changes in the viral genome in a
segment previously thought to be relatively stable. Epidemic neuropathy in
Cuba has features that suggest a combined nutritional/viral etiology.
Further research, both basic and applied, is needed to assess properly the
possible role of malnutrition in contributing to the emergence of novel
viral diseases.
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