Influenza A virus constitutes a serious health problem being responsible for a quarter to half a million deaths annually, depending on the pathogenicity of the circulating strain, prior immunity, and effectiveness of the administered vaccine.
Pathogenesis determinants include the intrinsic properties of IAV strains, and their interplay with host defence mechanisms. The Amorim lab found a specific interaction between influenza A virus and the complement system. With renewed interest caused by implementation of successful complement-targeting therapies, the complement is not just a pathogen killer, but a key player in immunity. It bridges innate and adaptive responses, and orchestrates the intensity of immunological and inflammatory processes by communicating with immune cells. Interactions are beginning to be fully appreciated, and their identification is crucial, as excess complement activation is associated with severe outcomes in many infections. In addition, the complement must be selective enough to avoid mounting a potent attack against the host. The self-targeting deleterious effects of complement are avoided via a series of so called regulators of complement activation (RCA). Our goal is to understand the role of these RCAs in influenza A virus infection, contributing to better define how complement communicates with other biological systems.