While the basic principles of immunity to the influenza A viruses are probably similar for all vertebrates, detailed understanding is based largely on experiments in laboratory mice. Elements of the innate response limit early virus replication, although high pathogenicity strains can trigger effusive cytokine/chemokine production and lethal shock. Virus clearance is normally mediated via CD8+ effector T cells but, in their absence, the class-switched antibody response can ultimately achieve the same goal. Protection against reinfection is optimally provided by antibody (IgG and IgA) specific for the homologous viral haemagglutinin, and priming against the neuraminidase and the low abundance, conserved M2 protein can also have an effect. Influenza virus-specific plasma cells and CD8+ T cells persist in the long term and the recall of the CD8+ T cell response can lead to earlier virus clearance. The characteristics of the aging immune system and possible, novel vaccine strategies are also considered.