Introduction Influenza virus infection produces a local inflammatory response that is characterized by edema and infiltration of inflammatory cells into the airway (1-5). This response occurs in association with desquamation of ciliated epithelial cells induced by replication of the influenza virus. The cells recruited into the airway in response to influenza infection consist of polymorphonuclear leukocytes and mononuclear cells (1, 2, 4, 6, 7). Recruitment of these cells continues throughout the course of infection into the recovery phase. Complement is a central mediator of inflammation and as such may play an important role in the local inflammatory response associated with influenza virus infection. As an essential first step in determining the involvement of complement in this response, we have asked the question: Does complement activation occur in the upper respiratory tract during experimental influenza virus infection in human volunteers? The results of our study document the presence of C3a and C5a in nasal lavage fluids from subjects who develop influenza illness.