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Initial genetic characterization of the S-OIV outbreak by the United States Centers for Disease Control suggested swine as its probable source, on the basis of sequence similarity to previously reported swine influenza isolates (CDC, 2009a). Classical swine H1N1 viruses have circulated in pigs in North America and other regions for at least 80 years (CDC, 2009a). In 1998, a new triple- reassortant H3N2 virus—comprising genes from classical swine H1N1, North American avian, and human H3N2 (A/Sydney/5/97-like) influenza—was reported as the cause of outbreaks in North American swine, with subsequent establishment in pig populations (CDC, 2009a; Shortridge et al., 1977). Co-circulation and mixing of the triple-reassortant H3N2 with established swine lineages subsequently generated further H1N1 and H1N2 reassortant swine viruses (CDC, 2009a; Shortridge et al., 1977; Shope and Lewis, 1931) which have caused sporadic human infections in the United States since 2005 (Newman et al., 2008; Shinde et al., in press). Consequently, human infection with H1N1 swine influenza has been a nationally notifiable disease in the United States since 2007 (CDC, 2009a,b). In Europe, an avian H1N1 virus was introduced to pigs (‘avian-like’ swine H1N1) and first detected in Belgium in 1979 (Pensaert et al., 1981; CDC, 2009a). This lineage became established and gradually replaced classical swine H1N1 viruses, and also reassorted in pigs with human H3N2 viruses (A/PortChalmers/1/1973-like) (CDC, 2009a). It is noteworthy that, until now, there has been no evidence of Eurasian avian-like swine H1N1 circulating in North American pigs. In Asia, the classical swine influenza lineage circulates, in addition to other identified viruses, including human H3N2, Eurasian avian-like H1N1, and North American triple-reassortant H3N2 (Peiris et al., 2001; Jung and Song, 2007; CDC, 2009a; Shortridge, 1977).

Using comprehensive phylogenetic analyses, we have estimated a temporal reconstruction of the complex reassortment history of the S-OIV outbreak, summarized in Fig. A14-1 (Methods). Our analyses showed that each segment of the S-OIV genome was nested within a well-established swine influenza lineage (that is, a lineage circulating primarily in swine for >10 years before the current outbreak). The most parsimonious interpretation of these results is therefore that the progenitor of the S-OIV epidemic originated in pigs. Some transmission of swine influenza has, however, been observed in secondary hosts in North America, for example, in turkeys (CDC, 2009a). Although the precise evolutionary pathway of the genesis of S-OIV is greatly hindered by the lack of surveillance data (see later), we can conclude that the polymerase genes, plus HA, NP and NS, emerged from a triple-reassortant virus circulating in North American swine. The source triple-reassortant itself comprised genes derived from avian (PB2 and PA), human H3N2 (PB1) and classical swine (HA, NP and NS) lineages. In contrast, the NA and M gene segments have their origin in the Eurasian avian-like swine H1N1 lineage. Phylogenetic analyses from the early days of the outbreak, on the basis of the first publicly available sequences, quickly established this multiple genetic origin (Novel Swine-Origin Influenza A (H1N1) Virus Investigation Team, in

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