Oxygen radicals and nitric oxide (NO) are generated in excess in a diverse array of microbial infections. Emerging concepts in free radical biology are now shedding light on the pathogenesis of various diseases. Free-radical induced pathogenicity in virus infections is of great importance, because evidence suggests that NO and oxygen radicals such as superoxide are key molecules in the pathogenesis of various infectious diseases.

It is becoming increasingly apparent that certain types of inflammatory tissue injury are mediated by reactive oxygen metabolites. The most likely sources of these oxidizing agents are the phagocytic leukocytes (e.g., neutrophils, monocytes, macrophages, and eosinophils) that invade the tissue. These reactive radicals and oxidants may injure cells and tissue directly via oxidative degradation of essential cellular components as well as injure cells indirectly by altering the protease/ antiprotease balance that normally exists within the tissue interstitium. It is becoming increasingly apparent that in addition to promoting cytotoxicity, reactive oxygen metabolites may also initiate and/or amplify inflammation via the upregulation of several different genes involved in the inflammatory response, such as those that code for proinflammatory cytokines and adhesion molecules.