Influenza viruses are negative stranded, segmented, enveloped RNA viruses belonging to the Orthomyxoviridae family and 3 virus types: A, B, and C exist. Influenza A and B are the main human pathogens whereas influenza C is rarely pathogenic for man and has no animal reservoir. Virus particles consist of three major components: the viral envelope, the matrix protein (M1), and the viral ribonucleocapsid. Three transmembrane envelope proteins: hemagglutinin (HA), neuraminidase (NA), and M2 are anchored in the lipid bilayer of the viral envelope. HA provides the receptor-binding site and elicits neutralizing antibodies. Cleavage of HA is essential for fusion and virus infectivity. NA removes the cell surface receptor (sialic acid) and is critical for the release of virus particles from the cell surface and spread of virus. M2 is a minor protein component of the viral envelope that functions as an ion channel crucial during uncoating. Influenza viruses are further classified into subtypes depending on the arrangements of the HA and NA surface glycoproteins. To date 16 HA subtypes (H1–H16) and 9 NA subtypes (N1–N9) have been identified. Human influenza viruses are limited to three HA (H1, H2, and H3) and two NA (N1 and N2) subtypes, whereas birds are the predominant hosts for the other subtype strains. Variations in these surface glycoproteins mean that new antigenic strains of influenza are continually appearing and account for the occurrence of yearly epidemics and pandemics. Variation can arise through the two processes of antigenic drift and antigenic shift. Antigenic drift occurs in both influenza A and B and involves the accumulation of point mutations in the surface glycoproteins, leading to the evolution of new strains of virus. The new strains are related to those circulating during preceding epidemics, but once evolved far enough away from preceding strains, the virus evades immune recognition which leads to repeated outbreaks. Antigenic shift occurs when mixed infection in animal hosts allows mixing of genes between different subtypes and therefore occurs with influenza A only, as B has no animal host. This process can result in major changes in the surface glycoproteins and emergence of a virus that is antigenically distinct from previous human viruses, allowing escape from herd immunity. As pigs can be infected with both human and avian influenza viruses, it is believed that this may be the source of new virus subtypes derived by antigenic shift. This can also occur in humans exposed to high levels of avian flu, or by gradual adaptation of an avian strain through repeated minor ‘forays’ into humans before it finally adapts sufficiently to ‘take off’. Antigenic shift is the process underlying the occurrence of influenza pandemics in human populations. Human influenza A viruses in the first half of this century carried H1N1 surface antigens but in 1957 the virus acquired the genes for the H2 and N2 antigens by reassortment of its genome with an avian virus. As the human population had no immunity to these new antigens the virus caused the ‘Asian flu’ pandemic. A similar antigenic shift gave rise to the H3N2 virus and the pandemic of 1968. The arrangement of the membrane proteins also influences the virulence of influenza strains. The H3N2 strain of influenza A is the most virulent of the recently circulating influenza viruses and the predominance of this strain during the 1990s may have been another important factor contributing to the increase in influenza-associated deaths.