There is historical evidence that three to four times a century severe worldwide epidemics (pandemics) of influenza occur. We know that the most recent of these were associated with the introduction into the human population of a subtype of influenza A that had not been experienced previously or, at least for several decades, and referred to as ‘antigenic shift'.
During the last century three pandemics, of somewhat different severity, occurred commencing in 1918 (Spanish flu), 1957 (Asian flu) and 1968 (Hong Kong flu). The 1918 pandemic is now thought to have claimed up to 50 million lives whereas those commencing in 1957 and 1968 may have accounted for around 1 and 2 million lives lost respectively. The world experienced a fourth pandemic in 2009, H1N1 pdm (Swine flu). The reported deaths were well over 16,000.
Molecular analyses, including some remarkable studies using preserved tissue samples from the Spanish flu outbreak, have provided valuable insights into the origins of the viruses causing these pandemics. The viruses responsible for the 1957 and 1968 pandemics were both genetic hybrids between the previously circulating human influenza A virus and a bird influenza A virus in which the pandemic virus acquired a new and distinct haemagglutinin protein from the bird virus (i.e. the virus became a new subtype). This probably facilitated the introduction of the new subtype into the human population as there are a number of hurdles that an influenza virus must overcome in successfully moving from one host to another. The human population had not experienced similar viruses therefore it was more susceptible to severe infection in comparison to the usual seasonal influenza strains created by mutation of previously circulating viruses (i.e. antigenic drift).
The 1957 virus inherited both a new haemagglutinin and new neuraminidase from the avian virus possibly explaining its greater severity compared with the 1968 virus. There are however indications that the Spanish flu did not go through this genetic mixing process but may have arisen directly by the adaptation of a bird influenza to humans. This may be a reason for its greater severity and could be relevant in terms of the observed severity of the avian H5N1 influenza in humans.
Genetic analyses of the 2009 H1N1pdm virus have shown that it originated from animal influenza viruses and is unrelated to the human seasonal H1N1 viruses that have been in general circulation among people since 1977. After early outbreaks in North America in April 2009 the new influenza virus spread rapidly around the world. Most of the deaths caused by the pandemic influenza have occurred among younger people, including those who were otherwise healthy.1
Due to the potential severity of pandemic influenza and the lead-time and limited capacity for vaccine production, WHO and national governments have formulated plans that are hoped to minimise the health care and economic impact of such an event.
Australian pandemic plan: http://www.health.gov.au/pandemic
Page publication: January 2014
Last updated: 27 June 2017