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• Original flu described in pigs by Shope in 1930 (earthworms) before human influenza.
• Original USA H1N1 in UK in 1941 then disappeared.
• Occurred in Europe in 1976 in Italy and then spread North and West.
• Mid 1980’s H1N1 in UK, mild, and most herds sero-converted without clinical signs.
• Mid 1980’s H3N2 human-like viruses arrived in pigs from direct transfer from humans (reverse zoonosis)-mild disease again except for the first few cases.
• These two viruses circulated widely until around 1991 when the wholly adapted poultry virus H1N1/Weybridge/195852 entered the pig population and since then it has largely replaced the original H1N1.
• In late 1990s a recombinant of avian virus (middle 6 genes) and human H1 and human N2, (from human viruses which had disappeared from humans but had remained in the pig reservoir over this period) appeared in the UK pig population, now known as H1N2
• In the past usually only 1 type (H1 or H3) was predominant at any one time, this is no longer so there is much more opportunity for mixing of viruses. This was true of man and pig.
• There have been isolated occurrences of other viruses but these have usually died out. Eg. H3N7 recombinant with a horse virus). The whole list would read H1N1, H1N2, H1N7, H2N3, H3N1, H3N2,H3N3, H3N8, H4N6, H5N1, H5N2, H9N2,
• In Europe the viruses are much the same (H1N1 and H1N2) but the genetics of the individual viruses differ from those of the UK.
• Europe uses swine influenza vaccines in pigs but these have never been licensed in the UK (Too small a population to make worth licensing, pushes the natural virus to change and you have to update the vaccine at regular intervals)
• AT THE MOMENT H1N1 (195852) AND H1N2 ARE THE TWO VIRUSES FOUND IN UK PIGS. POSSIBLY 40% OF HERDS AND 10-90% OF PIGS IN THE HERD ARE INFECTED DEPENDING ON SIZE AND MANAGEMENT ETC.
• World-wide there have been other incursions, usually locally into pigs eg H4 virus in Canada and particularly the H5N1 virus of poultry (the High Pathogenicity Avian influenza virus) which has adapted to pigs in South-east Asia and has now been shown to spread from pig to pig but not as yet as far as I know from pig to human.
• The swine influenza virus has 8 genes coding for 11 major proteins. The two major ones are the HA (haemagglutinin) and the NA (neuraminidase). They are responsible for infection and pathogenicity. These obviously are the major determinants of the type of virus (all mammalian viruses are influenza A). The other 6 genes are more incidental and often relate to structural proteins.
• The H gene exists in so many forms ;- 1-15. (The HA mediates the binding of influenza viruses to their target cell. Binding preference to specific sialylated glycan receptors is a critical determinant of H1N1 virus transmission efficiency in ferrets. The efficiency of respiratory droplet transmission correlates well with the alpha-2-.6 binding affinity of the viral HA.).
• The N gene exists in so many forms ;- 1-9
• These viruses change their genetics in three ways
a) antigenic drift – the virus undergoes abherrant replication ie mutationWe have had examples of all three types in the UK in recent years.
b) antigenic shift – where the virus swaps a complete gene with another virus
c) complete adaptation of a virus from another host into your species.
Over the years we have had a wide variety of swine viruses crop up in the world swine populations. They include H1N1, H1N2, H1N7, H2N3 (2006 in the USA), H3N1( in feeder pigs in Italy, in 2006), H3N2, H3N3, H3N8, H4N6, H5N1,H5N2 and H9N2.
It is also important to remember that an H1N2 in Europe may not be the same as an H1N2 in the USA.
In birds virtually all the combinations of HA and NA have been found to exist at some time. It is also important to remember that the virus principally infects the gastro-intestinal tract and viruses are shed in the faeces into any environmental site including pig houses and outdoor units.
• It is important to remember that each virus can only infect a host through receptors and in the case of the flu viruses there are two of these alpha-sialyl receptors known as 2.6 and 2.3. It was previously thought that the alpha 2.3 receptors were only found in the bird (particularly in the gut and avian influenza is primarily an alimentary disease) and the 2.6 receptors were found in the mammals. The pig was thought to be unusual in that it had both receptors. This gave rise to the idea that the pig was a “mixing vessel” for both mammalian and avian viruses.
• However, in the last few years it has been shown that pigs and humans also have both sets of receptors but 2.3s are more common in birds and the 2.6s more common in humans and pigs probably have similar numbers of both.
• Of equal importance, however in the respiratory tract alone the 2.3s occur in the upper respiratory tract and the 2.6s in the nose and conchal bones and many more 2.6s in the lung. In other words, not only are there species distribution differences, but there are also tissue tropisms.
• In the pig, as in the other species you do not find the flu virus in any other tissues other than those from the lung and rest of respiratory tract and it is eve difficult to recover from the thoracic lymph nodes if at all.
• It may have been overlooked until the recent analyses of both the human 1918 virus and the human 2009 virus that they exist in two forms – an upper respiratory tract form and a lower respiratory tract form ie the various strains of the virus attaché to different receptors in the respiratory tract. They differ slightly in their genomes
Human influenza
The 1918-19 influenza virus was believed to have gone from birds into humans and it is not known if it went from humans to pigs or pigs to humans.
The two most recent human pandemics were created from re-assortants of avian and human viruses. In 1957 H2N2 emerged in humans (3 genes from an avian virus and rest from a human) In1968, the H3N2 that emerged had 2 avian genes and the rest were from the previously circulating H2N2.
A recent paper reported in a review only approximately 50 cases of zoonotic swine influenza (Myers, K.P. et al 2007, Clin. Infect. Diseases, 44, 1084-1088.
