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THE outbreak of human pandemic influenza (H1N1) 2009 (pH1N1) that was first recorded in Mexico and then the USA in April 2009 spread to a number of countries in Europe and Asia (World Health Organization [WHO] 2009). The aetiological agent of pH1N1 is a reassortant virus that contains six gene segments from a North American triple-reassortant swine H1-subtype virus and the neuraminidase (NA) and matrix (M) genes from a Eurasian lineage H1N1 swine influenza. This latter virus existed in pigs around 10 to 20 years ago, as determined by Bayesian molecular clock analysis (Garten and others 2009, Smith and others 2009).
More recently, commercial pigs in Canada, Argentina, Australia, Singapore, Norway, the USA, Italy, Germany and the UK have been confirmed to be infected with the pH1N1 virus, suggesting efficient transmission between human beings as well as within pig populations (International Society for Infectious Diseases 2009). Pigs infected either artificially or naturally with pH1N1 show similar clinical signs to those of pigs infected with swine influenza A virus (SIV). Clinical signs vary from mild (characterised by depression, fever, sneezing and nasal discharge) to inapparent (Hofshagen and others 2009, Howden and others 2009, Brookes and others 2010, Pasma and Joseph 2010, Weingartl and others 2010, Welsh and others 2010). Reports suggest that in most of these cases, pH1N1-infected human beings transmitted the virus to pigs; however, in some cases in Canada, pigs were suspected to have infected other pigs directly (International Society for Infectious Diseases 2009, Pasma and Joseph 2010).
Before the emergence of pH1N1 in South Korea, H1N1, H1N2 and H3N2 SIVs were the principal viruses isolated from pig populations (Lee and others 2008). However, due to its low mortality and economic impact, swine influenza was not designated as a nationally …
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