Swine flu

Viruses of the H1N1, H1N2 and H3N2 subtypes have commonly originated in pig populations in various parts of the world.

The pandemic H1N1 2009 virus, which emerged in the human population in north America then rapidly spread worldwide was a virus from pigs that had genes from viruses circulating in pigs in North America and genes from viruses circulating in Europe.

Since 1998 the viruses circulating in North America have been principally 'triple reassortants', deriving genes from classical swine (NP, M and NS), human (PB1) and avian (PB2 and PA) viruses. The HA and NA genes of the H1N1 viruses that were circulating in pigs were derived from classical swine H1N1 viruses, those of the H3N2 viruses from contemporary human viruses, and those of the H1N2 viruses from classical swine and human viruses, respectively. Since 2005, H1N1 and H1N2 subtypes, which derived their HA and NA genes from human viruses, have also co-circulated. The triple reassortant viruses contributed six genes to the H1N1pdm09 virus: the PB2 gene, the PB1, gene, the PA gene, the HA gene, the NP gene and the NS gene. Since the 2009 human pandemic, the human pandemic virus H1N1pdm09 has also circulated in pigs. Reassortment between the H1N1pdm09 viruses and H1N1 and H3N2 and H1N2 viruses from pigs has occurred.

In Europe, H1N1 viruses are descended from an avian virus introduced into pigs in the late 1970s. This virus contributed two genes to the H1N1pdm09 virus, the gene encoding the NA and the M gene segment encoding M1 and M2 . Two other subtypes circulating in pigs, H1N2 and H3N2 viruses are closely related in their six internal genes, due to frequent genetic exchange between viruses of the different subtypes. The H1 of H1N2 viruses, which emerged in the UK in the early 1990s, is descended from H1N1 viruses circulating in the human population in the early 1980s, while the H3 and N2 components are descended from H3N2 swine viruses closely related to early human H3N2 viruses. In many countries in Europe H1N1pdm09 viruses have become established in pigs.

Several examples of sporadic human infection by some of these swine viruses, in Europe, North America and elsewhere have been reported in recent years. Although there has been evidence for limited human-to-human transmission, these viruses have not transmitted efficiently between people. Of note is that swine influenza viruses in North America that have acquired the M gene from H1N1pdm09 has resulted in human infections. Primarily these have been swine H3N2 viruses and are termed H3N2v viruses for variant H3N2 viruses. Over 300 cases of H3N2v infections have been detected, with smaller numbers of H1N1v and H1N2v infections, from viruses that also have acquired the M gene from the H1N1pdm09 virus, also detected.

A characteristic feature of viruses circulating in pigs in Europe since the mid 1980s and the human pandemic H1N1 2009 viruses is their resistance to the anti-influenza A drugs, amantadine and rimantadine, due to the presence of asparagine at position 31 of the M2 channel. The viruses are sensitive to the anti-neuraminidase drugs, zanamivir and oseltamivir.