Swine Influenza by Jürgen A. Richt & Richard J. Webby

Author:Jürgen A. Richt & Richard J. Webby
Language: eng
Format: epub
Publisher: Springer Berlin Heidelberg, Berlin, Heidelberg

It is thought that the pandemic virus of humans was also the causative strain that infected swine populations around the same time, as indicated by the close relatedness of the isolated strains, but these viruses had evolved separately in each host after the pandemic (Shope 1931). This swine virus, known as the “classical” H1N1 swine virus, continued to be found in pigs in the United States and Asia, but it was not found in Europe until 1980 (Pensaert et al. 1981; Peiris et al. 2009a). After the Hong Kong influenza pandemic in 1968, the wholly human-like H3N2–subtype virus (a non-reassorted H3N2 strain bearing segments identical to the virus circulating among humans) was transmitted to pigs and was initially detected in a Taiwanese slaughterhouse in 1969 (Kundin 1970; Shortridge et al. 1977). This originally avian–human reassortant virus continued to circulate in Europe and Asia; it was only infrequently found in North America before 1998, causing sporadic clinical signs (Chambers et al. 1991; Webby et al. 2000; Yu et al. 2008). The reemergent H1N1 virus in 1977 (Russian flu) that affected young adults and genetically closely resembled viruses of the early 1950s (Nakajima et al. 1978) was also isolated from pigs in Europe and Asia (Alexander 1982).

In North America, the “classical” swine H1N1 virus continued to be predominant over the sporadically detected Hong Kong H3N2 human virus in circulation among swine populations until 1998 (Hinshaw et al. 1978; Chambers et al. 1991; Karasin et al. 2000b). However, by late August 1998, two distinct genotypes of H3N2 influenza virus had emerged, caused outbreaks, and spread rapidly in North American swine populations (Zhou et al. 1999; Karasin et al. 2000c; Webby et al. 2000). These viruses were either double reassortant virus (i.e., HA, NA, and PB1 genes of human H3N2 and PB2, PA, NP, M, and NS genes of classical swine H1N1) or triple reassortant virus (i.e., human H3N2-classical swine H1N1 virus with PB2 and PA genes of a North American avian virus) (Zhou et al. 1999). Eventually, only the triple reassortant internal gene (TRIG) cassette virus continued to circulate and became established. Shortly after its emergence, cocirculation of this H3N2-reassortant virus with the previously predominant classical swine H1N1 virus resulted in the production of a reassortant H1N2 virus subtype that retained the entire TRIG backbone and acquired the HA gene of classical swine H1 (Karasin et al. 2000b). This lineage of reassortant H1N2 viruses has subsequently spread widely among North American pigs and is often associated with respiratory disease, although some strains have caused spontaneous abortion in sows (Choi et al. 2002a; Karasin et al. 2002). Reassortant H1N2 and H3N2 SIVs carrying the TRIG cascade have also been found in domestic turkey populations (Suarez et al. 2002; Choi et al. 2004a), and the H1N2 virus alone has been detected in wild waterfowl (Olsen et al. 2003; Ramakrishnan et al. 2010). In humans, 11 patients in the United States have been confirmed to be infected with triple-reassortant H1 SIVs since 2005 (Shinde et al. 2009).

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