Oxygen Free Radicals as Pathogenic Molecules in Viral Diseases

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Abstract
Oxygen free radicals such as superoxide anion (O2-) were generated markedly in influenza virus-infected mouse lung, and these molecular species were identified as the potent pathogenic agents. This finding has many important implications for understanding viral pathogenesis: namely, the direct viral cytotoxicity (referred cytopathic effect) is only a fraction of several types of events induced by virus infection. The toxicity and reactivity of oxygen radicals, which are presumably generated in excessive amounts by the overreaction of the host's immune response against the organs or tissues in which viruses are replicating, may explain the mechanism of tissue injuries observed not only in influenza virus infection in mice, but also in other types of viral diseases in which immunological interactions are usually involved. Conclusion It has become clear that O2- is the prime toxic molecule generated in the viral infection. The generation of O2- is sustained by an enhanced supply of catabolic products of ATP and the much-elevated activity of the enzymes involved in this catabolic cascade. In fact, this suggestion was supported by the improved survival of mice when xanthine oxidase was inhibited. Likewise, Cu, Zn-SOD with longer plasma half-life and better biocompatibility, which removes toxic O2-, conferred a remarkably protective effect on the infected mice. A similar clinical consequence may be found in the symptoms of other viral diseases.

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