Fig. 5. Influenza antigenic shift and antigenic drift.

In 1968, co-infections between an avian influenza A H3Nx (where x = 1–9) virus and the seasonal human influenza A H2N2 viruses resulted in the exchange of viral segments (reassortment) and the selection of the pandemic human influenza A H3N2 virus, with the RNA polymerase PB1 and haemagglutinin (HA) RNA segments derived from the avian virus and the rest of the segments derived from the human virus. The lack of pre-existing immunity to the antigenically novel H3 HA in humans facilitated human transmission. Similar reassortment processes have taken place during other influenza A virus pandemics. Once H3N2 became established in humans, the virus began to drift, as is the case with all other human seasonal influenza viruses. During drift, small antigenic changes in the HA protein generated by mutation are selected to increase immune evasion, although not as dramatically as during shift. M, RNA encoding M1, matrix protein, and M2, membrane protein; NA, RNA encoding neuraminidase; NP, RNA encoding nucleoprotein; NS1, RNA encoding nonstructural protein; PB2 and PA, RNA encoding RNA polymerases.