Key result
Dietary oxidative stress from selenium or vitamin E deficiency increased cardiac damage in mice infected with coxsackievirus B3 and caused a benign strain to mutate to virulence.
Host nutritional deficiency (selenium or vitamin E) can induce oxidative stress that alters the genetic sequence of a viral pathogen, converting a benign virus into a virulent, heart-damaging strain.
Hypothesis-generating for nutritional modulation of viral virulence; requires human trials before any practice change.
Oxidative stress is implicated in the pathogenesis of several viral infections, including hepatitis, influenza, and AIDS. Dietary oxidative stress due to either selenium or vitamin E deficiency increases cardiac damage in mice infected with a myocarditic strain of coxsackievirus B3. Such dietary oxidative stress also allows a normally benign (i.e., amyocarditic) coxsackievirus B3 to convert to virulence and cause heart damage. This conversion to virulence is due to a nucleotide sequence change in the genome of the benign virus, which then resembles more closely the nucleotide sequence of virulent strains. Although it has been known for many years that poor nutrition can affect host response to infection, this is the first report of host nutrition affecting the genetic sequence of a pathogen. Further research is needed to determine whether poor host nutrition plays any role in the emergence of new viral diseases via alterations in he genotype of an infectious agent.
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Beck et al. (1998) studied Coxsackievirus B3 infection. Dietary oxidative stress (selenium or vitamin E deficiency) was evaluated on Cardiac damage and viral genetic sequence change. Dietary oxidative stress from selenium or vitamin E deficiency increased cardiac damage in mice infected with coxsackievirus B3 and caused a benign strain to mutate to virulence.
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