Although HMGB1 can be released by macrophages in response to viral infection [23], the gradual increase of HMGB1 observed in this study is considered to be induced by passive release from necrotic alveolar type II epithelial cells [5] and by active secretion from alveolar macrophages in response to TNFα, IL-1, IFNγ, and oxidative stress without proved molecular mechanisms [24–26]. Here, IFNG is linked to viral infectious disease.