Many viruses are capable of inducing reactive oxygen species (ROS) production. Results from many studies suggest that ROS are not directly involved in the induction of apoptosis in virus-infected cells [11, 12] . On the other hand, it has been demonstrated that virus infection increases the production of superoxide anion radicals from neutrophils and macrophages infiltrated into the lung of mice [13] , while transgenic mice carrying over-expressed extracellular superoxide dismutase exhibited less severe lung injury after influenza virus infection [14] . These studies, therefore, postulated that the pathogenesis of virus infection involves not only the virus proliferation mediated apoptotic cell death in the infected cells, but also the direct ROS-induced cellular injury by neutrophils and macrophages infiltrated into the virus-infected organs. But, despite many studies, the events leading to the generation of ROS during viral infections are still unclear.