Science for Health
Viruses of the H1N1, H1N2 and H3N2 subtypes have recently circulated in pig populations in various parts of the world.
In Europe, the current H1N1 viruses are descended from an avian virus introduced into pigs in the late 1970s. The two other subtypes are closely related in their 6 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.
Since 1998 the viruses circulating in North America have been principally “triple reassortants” deriving common 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 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 cocirculated. Similar viruses have since circulated also in countries in east Asia.
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.
The pandemic H1N1 2009 virus, which emerged recently in the human population in north America and has spread worldwide, derived six of its genes from 'triple reassortants' and its NA and M genes from swine viruses of the Eurasian lineage. The origin of these viruses is unknown. Two instances of the emergence in pig herds in Canada and Argentina have subsequently been reported.
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.
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