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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
3                           Triple-reassortant swine influenza A (H1) viruses--containing genes from av
4 o prevent an influenza epidemic from another swine influenza A H1N1 recombinant virus.
5                      After a new reassortant swine influenza A H1N1 virus caused outbreaks in Mexico
6 pin-enhanced DFA detected 230 (84.6%) of 272 swine influenza A PCR-positive results overall but 25 (9
7  immune responses and the major component in swine influenza A vaccines.
8                                   Control of swine influenza A virus (IAV) in the United States is hi
9 luate the efficacy of commercial inactivated swine influenza A virus (IAV) vaccines and experimental
10                                              Swine influenza A virus is an endemic and economically i
11                                              Swine influenza A viruses (IAV) are a major cause of res
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
14 cific for the detection of human, avian, and swine influenza A viruses.
15 s are higher than those of human and classic swine influenza A viruses.
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 (
20                   Concern that pandemic H1N1 swine influenza could be transmitted by solid organ tran
21  ecobiological association between human and swine influenza could extend to before 1918.
22 918, but an anecdotal report suggests that a swine-influenza epizootic might have occurred in England
23 gin reassortant containing human, avian, and swine influenza genes.
24 A/New Caledonia/20/99 [Ncal99]), a classical swine influenza H1N1 virus isolate (A/Swine/Iowa/15/30 [
25 lowing in vitro infection with 2009 pandemic swine influenza (H1N1/09).
26                                              Swine influenza has been recognised only since 1918, but
27                                          The Swine Influenza Immunization Program began in January 19
28                   Drawing from the ill-fated swine influenza immunization program of 1976, this artic
29 By contrast with the recent documentation of swine influenza, influenza in horses has been well docum
30                                              Swine influenza is a highly contagious zoonotic disease
31                                              Swine influenza is an acute respiratory disease caused b
32 lly poorly transmitted between humans, while swine influenza is better transmitted due to glycan simi
33                                   Control of swine influenza is primarily through the vaccination of
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
38                        In 1976, the national swine influenza vaccination program in the United States
39 drome (GBS) occurred among recipients of the swine influenza vaccine in 1976-1977.
40 e (GBS) following administration of the 1976 swine influenza vaccine led to a heightened focus on GBS
41       Vaccination with the A/New Jersey/1976 swine influenza vaccine substantially boosted cross-reac
42 ain-Barre Syndrome (GBS) found with the 1976 swine influenza vaccine, both active surveillance and en
43 tantially lower than that seen with the 1976 swine influenza vaccine.
44   GBS has also been associated with the 1976 swine-influenza vaccine.
45 were vaccinated with recent seasonal or 1976 swine influenza vaccines.
46 lb09]), with that of the 1918-like classical swine influenza virus (A/swine/Iowa/1930 [IA30]) in the
47                                   In 2009, a swine influenza virus (pH1N1) jumped to humans and sprea
48                                              Swine influenza virus (SIV) H3N2 with triple reassorted
49 1-F2 protein of triple-reassortant (TR) H3N2 swine influenza virus (SIV) in pigs and turkeys.
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
53 ation of a so-called triple reassortant (TR) swine influenza virus (SIV).
54                                              Swine influenza virus (SwIV) is one of the important zoo
55               As a positive control, an H3N2 swine influenza virus A was used.
56 y shown to enhance the replication of a 1976 swine influenza virus also significantly improved the re
57                Novel triple-reassortant H3N2 swine influenza virus emerged in 1998 and spread rapidly
58 n that infection in humans with the pandemic swine influenza virus induces antibodies with specificit
59                                 Before 1998, swine influenza virus isolates in the United States were
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 (
64 in A/New Caledonia/20/1999 and 2009 pandemic swine influenza virus strain A/California/04/2009.
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
70                   Therefore, we chose a H1N1 swine influenza virus, Sw/OH/24366/07 (SwIV), which has
71                             Unlike classical swine influenza virus, TR SIV produces a full-length PB1
72 onstrate here that an engineered reassortant swine influenza virus, with the same gene constellation
73                               We report that swine influenza virus-like substitutions T200A and E227A
74               A new H1N1 triple-reassortant "swine" influenza virus was recently described in individ
75 e its absence from some animal (particularly swine) influenza virus isolates, variable expression in
76                                              Swine influenza viruses (SIV) have been shown to sporadi
77                                              Swine influenza viruses (SIV) naturally infect pigs and
78                           Triple reassortant swine influenza viruses (SIVs) and 2009 pandemic H1N1 (p
79               Since the introduction of H3N2 swine influenza viruses (SIVs) into U.S. swine in 1998,
80                             We identified 34 swine influenza viruses (termed rH3N2p) with the same co
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
85 fluenza subtypes by mixing avian, human, and swine influenza viruses is possible.
86        Due to their attenuation, NS1-mutated swine influenza viruses might have a great potential as
87 e epitopes in parallel lineages of human and swine influenza viruses that have been diverging since r
88         Here we use comparisons of human and swine influenza viruses to rigorously demonstrate that h
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
96 l cells which is characteristic for virulent swine influenza viruses.
97 modon hispidus) are susceptible to avian and swine influenza viruses.
98 nd might reassort with currently circulating swine influenza viruses.
99 es and antigenically distinct from reference swine influenza viruses.
100  understanding of the antigenic diversity of swine influenza will facilitate a rational approach for

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