Immunohistochemical examination revealed the presence of viral antigens in the bronchioles, terminal bronchiolar epithelium, and alveolar epithelial cells. Perhaps SD/09 virus infection of the alveoli, particularly type II pneumocytes, rather than bronchioles, is a key to the development of ARDS. Type II pneumocytes are responsible for the production and secretion of surfactant to lower the surface tension of water and allow membrane separation, and insufficient pulmonary surfactant in the alveoli may result in alveolar collapse [28, 29] . The 1918 pandemic H1N1 and high pathogenic H5N1 viruses preferentially infect type II pneumocytes and alveolar macrophage in mice [15, 30] . Alveolar macrophages may play a critical role in disease pathogenesis, not through production of infectious virus but rather through the upregulation of proinflammatory cytokines that may further damage alveolar pneumocytes [31] . These phenomena suggest that viral cell tropism may determine the processes of ARDS.