The male-to-female ratio was 1.1:1 among all patients, and 1.6:1 among the admitted patients. Furthermore, male patients were predominant among those with pneumonia (3:1, 60/80) and those with respiratory distress who received corticosteroids (3.3:1, 13/17). Other epidemiologic studies on children have reported a male predominance [16] , but some studies on inpatients have reported a female predominance [4, 7] . These findings suggest that genetic factors and possibly environmental factors are Regarding the pathogenesis of lung injury in influenza virus infections, it has been believed that the viruses from upper respiratory tract spread to lower lung tissues and elicit the cytopathic reaction. However, some clinical and experimental studies have suggested that the innate and/ or cell-mediated immune reaction (T cell) with excessive production of cytokines of the host may also be responsible for the lung injury in influenza virus infection [9, [22] [23] [24] [25] . We experienced no intensive care patient in this series despite large subjects of the study, and it may be, at least in part, explained by a rapid use of corticosteroids on the patients with severe pneumonia [9, 10] . Because this pandemic occurred over 40 years after last pandemic (Hong Kong flu), there have been no controlled-clinical trials for the efficacy of corticosteroids on influenza virus infections, although yearly seasonal influenza and small cases of sporadic H5N1 avian influenza virus infection have occurred during inter-pandemic period. The beneficial effect of corticosteroids in pneumonia caused by influenza virus infections may have resulted from reduction of systemic inflammation caused by immune cells and cytokines [26, 27] . Our treatment policy which needs to be proven by controlled clinical studies in coming pandemics or in other influenza virus infections, may help to reduce the morbidity and possibly prevent the progression to fatal pneumonia [9, 10] . We have reviewed the rationale of our corticosteroid treatment and the host immune responses to viral insults in influenza virus infections, and proposed a new concept for the pathogenesis of acute lung injury in influenza virus infections, using a 'protein homeostasis system' of the host [9] .