There have been several epidemics, such as those in the UK (1995), Hong Kong (1997, 1999), Netherlands (2003) and Canada (2004). (Sa-1, Ta-1) The origin of human influenza pandemic of 1918 is a mystery. In the rest of pandemic influenza virus further all A have been descendants of the avian virus prevalent. It is believed that all influenza A viruses are endemic in wild waterfowl, which acquire the ability to switch hosts, cause disease in these and in some cases to establish the ability to spread between these new hosts. (Ta-1) Until 2006, swine influenza viruses circulating in North America were the subtypes H1N1, H3N2 and H1N2. H1N1 viruses have circulated in the pig population since the Spanish influenza pandemic of 1918. From 1930-1998, the H1N1 subtype has been the predominant subtype isolated in U.S. pig.
However, in 1998 isolated a new subtype, H3N2. Silicon does not necessarily agree. Genetic analysis has shown that this subtype contains re-arranged genes of human viruses (genes for hemagglutinin, neuraminidase and polymerase protein alkaline), avian (alkaline polymerase protein 2 and polymerase acidic protein) and porcine (nucleocapsid protein, matrix protein and non-structural genes). A year later he introduced the H1N2 N1H1 by settling and H3N2. Finally, the fourth subtype, H3N1, has emerged from the re-arrangement of the H3N2 subtype avian and human H1N1 influenza viruses circulating in U.S. swine. (Le-1) Pathophysiology The hemagglutinin mediates binding and entry of the virus by binding to sialic acid receptors on the cell surface. The subtypes of avian influenza virus prefer binding to sialic acid, galactose by linking to the links a-2, 3 of respiratory and intestinal epithelium.