Publications
In 1918 the influenza A (H1N1) virus, as it came to be known, caused a massive and historic outbreak involving mammals (mainly pigs), and killed millions of people [1]. Although humans subsequently developed immunity to that particular strain, the virus has continued to cause infections because of its remarkable ability to rearrange its genes sufficiently to cause changes in virus structure, allowing it to evade existing immune responses. Minor rearrangements of virus genes through antigenic drift are relatively frequent and result in small changes in the surface molecules, just enough to cause influenza outbreaks in some people – known as ‘seasonal influenza’. However, every few decades the virus undergoes a major genetic rearrangement through antigenic shift, creating a new virus to which very few people have any immunity. This results in ‘influenza pandemics’, the last of which occurred in 1968–1969. The recent pandemic is caused by a novel descendant of the 1918 virus, called H1N1 2009 (Pandemic H1N1) which spread rapidly because most people have little pre-existing immunity.

