Evolution of Swine H3N2 Influenza Viruses in the United States

Webby, Richard J.; Swenson, Sabrina L.; Krauss, Scott; Gerrish, Philip J.; Goyal, Sagar M.; Webster, Robert G.

doi:10.1128/jvi.74.18.8243-8251.2000

Cited by 333 publications

(285 citation statements)

References 34 publications

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“…The classical SIV (cH1N1), which is similar to the human 1918 pandemic virus, remained antigenic and genetically conserved in the United States until the introduction of an H3N2 virus in 1998 5. The cocirculation of cH1N1 and the H3N2 virus led to reassortment and resulted in the introduction of the reassorted H3N2, H1N1,6 and H1N2 subtypes 7. Reassortant viruses currently endemic in North American swine have combinations of different HA and NA genes with a triple‐reassortant internal gene (TRIG) cassette formed by the human lineage PB1 gene, the avian lineage PA and PB2 genes, and the classical swine lineage M, NP, and NS genes 5.…”

Section: Introductionmentioning

confidence: 99%

Genetic characterization of influenza virus circulating in Brazilian pigs during 2009 and 2010 reveals a high prevalence of the pandemic H1N1 subtype

Rajão

Costa

Brasil

et al. 2012

Influenza Resp Viruses

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BackgroundInfluenza A viruses circulating in pigs in Brazil are still not characterized, and only limited data are available about swine influenza epidemiology in the country. Therefore, we characterized the hemagglutinin (HA) and neuraminidase (NA) genes of influenza viruses isolated from Brazilian pigs. We also evaluated one case of probable swine‐to‐human transmission.MethodsTwenty influenza viruses isolated from pigs during 2009–2010 in five Brazilian states (Minas Gerais, Sao Paulo, Parana, Rio Grande do Sul, and Mato Grosso) were used. One human isolate, from a technician who became ill after visiting a swineherd going through a respiratory disease outbreak, was also used in the study. Phylogenetic analysis for the HA and NA genes and hemagglutinin amino acid sequence alignment were performed.ResultsAll isolates clustered with pandemic H1N1 2009 (pH1N1) viruses and appeared to have a common ancestor. Genetic diversity was higher in the HA than in the NA gene, and the amino acid substitution S203T in one of HA's antigenic sites was found in most of the samples. The human isolate was more related to swine isolates from the same herd visited by the technician than to other human isolates, suggesting swine‐to‐human transmission.ConclusionOur results show that pH1N1 was disseminated and the predominant subtype in Brazilian pigs in 2009–2010.

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Section: Introductionmentioning

confidence: 99%

Genetic characterization of influenza virus circulating in Brazilian pigs during 2009 and 2010 reveals a high prevalence of the pandemic H1N1 subtype

Rajão

Costa

Brasil

et al. 2012

Influenza Resp Viruses

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“…Two of these isolates were from individuals that had documented exposure to swine and were infected by ''triple reassortant'' viruses containing human PB1, avian PB2 and PA, and classic swine NP, similar to the 2009 A(H1N1 viruses) (22,23). The SR polymorphism is more prevalent in pigs, present in Ͼ20% of the sequenced isolates, but only appears after the establishment of the triple reassortant swine viruses that emerged in 1998-1999 (24,25). For all isolates, the SR polymorphism occurs only when there is also the E627 variant.…”

Section: Srmentioning

confidence: 99%

Adaptive strategies of the influenza virus polymerase for replication in humans

Mehle¹,

Doudna

2009

Proc. Natl. Acad. Sci. U.S.A.

343

373

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Transmission of influenza viruses into the human population requires surmounting barriers to cross-species infection. Changes in the influenza polymerase overcome one such barrier. Viruses isolated from birds generally contain polymerases with the aviansignature glutamic acid at amino acid 627 in the PB2 subunit. These polymerases display restricted activity in human cells. An adaptive change in this residue from glutamic acid to the human-signature lysine confers high levels of polymerase activity in human cells. This mutation permits escape from a species-specific restriction factor that targets polymerases from avian viruses. A 2009 swineorigin H1N1 influenza A virus recently established a pandemic infection in humans, even though the virus encodes a PB2 with the restrictive glutamic acid at amino acid 627. We show here that the 2009 H1N1 virus has acquired second-site suppressor mutations in its PB2 polymerase subunit that convey enhanced polymerase activity in human cells. Introduction of this polymorphism into the PB2 subunit of a primary avian isolate also increased polymerase activity and viral replication in human and porcine cells. An alternate adaptive strategy has also been identified, whereby introduction of a human PA subunit into an avian polymerase overcomes restriction in human cells. These data reveal a strategy used by the 2009 H1N1 influenza A virus and identify other pathways by which avian and swine-origin viruses may evolve to enhance replication, and potentially pathogenesis, in humans.2009 A(H1N1) ͉ PB2 ͉ species barriers

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“…The initial North Carolina isolate (double reassortant) contained gene segments similar to those of the human (HA, NA, PB1) and classical-swine (NS, NP, M, PB2, PA) lineages, whereas the isolates from Minnesota, Iowa, and Texas (triple reassortant) contained genes from the human (HA, NA, PB1), swine (NS, NP, M), and avian (PB2, PA) lineages (Zhou et al, 1999). By the end of 1999 viruses antigenically and genetically related to the triple reassortant lineage were widespread in the US swine population Webby et al, 2000).…”

Section: Introductionmentioning

confidence: 99%