Key result
Oxidative stress exacerbated viral pathogenesis, with a coxsackie-like virus isolated from 84% of cultured patients during a neuropathy epidemic linked to antioxidant deficiency.
Oxidative stress can exacerbate viral pathogenesis and induce viral genome changes, potentially leading to severe manifestations such as myocarditis.
Antioxidant deficiency may worsen viral outcomes in deficient populations; leaves open whether repletion alters pathogenesis or clinical severity.
Oxidative stress is implicated as a pathogenic factor in a number of viral infections. Our work has shown that nutritionally induced oxidative stress exacerbates the pathogenesis of coxsackievirus B3 (CVB3) infection in mice. Of particular note, mice fed on a diet deficient in antioxidants developed myocarditis when infected with a normally benign strain of CVB3. This change in virulence was found to be due to changes in the viral genome. Immune functions of the oxidatively stressed mice were also altered. Another example of the effect of oxidative stress on a viral pathogen took place in Cuba in the 1990s. An epidemic of optic and peripheral neuropathy in the population occurred that was associated with a lack of dietary antioxidants and with smoking (a pro-oxidant). A coxsackie-like virus was isolated from the cerebrospinal fluid from 84% of patients cultured. Thus, oxidative stress can have profound effects, not only on the host, but on the pathogen as well.
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Beck et al. (2000) conducted a review in Viral infections (coxsackievirus B3, optic and peripheral neuropathy). Oxidative stress (antioxidant deficiency and smoking) was evaluated. Oxidative stress exacerbated viral pathogenesis, with a coxsackie-like virus isolated from 84% of cultured patients during a neuropathy epidemic linked to antioxidant deficiency.
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