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1 s sporadic infection with triple-reassortant swine influenza A (H1) viruses in persons with exposure
2 infection of humans with triple-reassortant swine influenza A (H1) viruses reported to the Centers f
6 pin-enhanced DFA detected 230 (84.6%) of 272 swine influenza A PCR-positive results overall but 25 (9
9 luate the efficacy of commercial inactivated swine influenza A virus (IAV) vaccines and experimental
12 additional 1,404 whole-genome sequences from swine influenza A viruses collected globally during 1931
13 s are evidently more resistant to avian than swine influenza A viruses, mediated in part through fron
16 ed to assess persistence of antibody against swine influenza A/H1N1(2009) pandemic influenza, childre
17 am began in January 1976 with an outbreak of swine influenza among trainees at Ft. Dix, New Jersey.
18 rigins of the pandemic virus and the classic swine influenza and (postpandemic) seasonal H1N1 lineage
19 69 ferrets infected with seasonal influenza, swine influenza, and highly pathogenic avian influenza (
22 918, but an anecdotal report suggests that a swine-influenza epizootic might have occurred in England
24 A/New Caledonia/20/99 [Ncal99]), a classical swine influenza H1N1 virus isolate (A/Swine/Iowa/15/30 [
29 By contrast with the recent documentation of swine influenza, influenza in horses has been well docum
32 lly poorly transmitted between humans, while swine influenza is better transmitted due to glycan simi
34 2009 virus was derived from well-established swine influenza lineages; however, there is no convincin
35 ity to pandemic H1N1 hemagglutinin after the swine influenza pandemic of 2009 in pooled human polyclo
36 luenza A virus strains, such as the new H1N1 swine influenza, represents a serious threat to global h
37 lCer generates protective immunity against a swine influenza (SI) virus infection when applied as an
40 e (GBS) following administration of the 1976 swine influenza vaccine led to a heightened focus on GBS
42 ain-Barre Syndrome (GBS) found with the 1976 swine influenza vaccine, both active surveillance and en
46 lb09]), with that of the 1918-like classical swine influenza virus (A/swine/Iowa/1930 [IA30]) in the
50 raction between Mycoplasma hyopneumoniae and swine influenza virus (SIV) in the induction of pneumoni
51 dentifying a student with triple-reassortant swine influenza virus (SIV) infection and pig exposure a
52 ole of the NS1 protein in the virulence of a swine influenza virus (SIV) isolate in pigs by using rev
56 y shown to enhance the replication of a 1976 swine influenza virus also significantly improved the re
58 n that infection in humans with the pandemic swine influenza virus induces antibodies with specificit
60 recursor strains from the triple-reassortant swine influenza virus lineage, which cause only sporadic
61 , and nonstructural genes being of classical swine influenza virus origin, and the PA and PB2 polymer
62 The recent flu epidemic caused by an H1N1 swine influenza virus presents an opportunity to examine
63 Biosystems 7500 Fast platform, using the CDC swine influenza virus real-time RT-PCR detection panel (
65 rotected completely against lethal avian and swine influenza virus strains in mice, and induced robus
66 to a representative human triple-reassortant swine influenza virus that has circulated in pigs in the
67 ls which recovered from exposure to virulent swine influenza virus were completely resistant to infec
68 th the reconstructed 1918 virus, a 1976 H1N1 swine influenza virus, and a highly pathogenic H5N1 viru
69 CD8(+) T-cell epitopes in NP of human versus swine influenza virus, consistent with the idea that the
72 onstrate here that an engineered reassortant swine influenza virus, with the same gene constellation
75 e its absence from some animal (particularly swine) influenza virus isolates, variable expression in
81 logic factors that limit the transmission of swine influenza viruses between humans are unresolved.
82 large-scale genomic characterization of 290 swine influenza viruses collected from 14 European count
83 ttle known about the host barriers that keep swine influenza viruses from entering the human populati
84 se data highlight the increased diversity of swine influenza viruses in the United States and would i
87 e epitopes in parallel lineages of human and swine influenza viruses that have been diverging since r
89 y (typically found in avian and classic H1N1 swine influenza viruses), conferring binding to human- a
90 uman H1N1 influenza A virus strains, several swine influenza viruses, and influenza B viruses but wer
91 uenza viruses, unlike other human, avian and swine influenza viruses, are resistant to the antiviral
92 nes can be recombined from human, avian, and swine influenza viruses, leading to triple reassortants.
93 However, when transferred into avian and swine influenza viruses, only partial ts and attenuation
94 ing a panel of 28 distinct human, avian, and swine influenza viruses, we found that only a small subs
95 ses--containing genes from avian, human, and swine influenza viruses--emerged and became enzootic amo
100 understanding of the antigenic diversity of swine influenza will facilitate a rational approach for
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