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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  H9N2) and publications describing emergence swine Influenza A cases in humans together with "G4" Eur
5 o prevent an influenza epidemic from another swine influenza A H1N1 recombinant virus.
6                      After a new reassortant swine influenza A H1N1 virus caused outbreaks in Mexico
7 pin-enhanced DFA detected 230 (84.6%) of 272 swine influenza A PCR-positive results overall but 25 (9
8  immune responses and the major component in swine influenza A vaccines.
9 terized the antigenic evolution of the N2 of swine influenza A virus (IAV) across 2 decades following
10                                   Control of swine influenza A virus (IAV) in the United States is hi
11 luate the efficacy of commercial inactivated swine influenza A virus (IAV) vaccines and experimental
12 ole-inactivated virus (WIV) vaccines against swine influenza A virus (IAV).
13                                              Swine Influenza A Virus (IAV-S) poses a significant burd
14                                              Swine influenza A virus (swIAV) infection causes substan
15                                              Swine influenza A virus (swIAV) is an important zoonotic
16 n 2009, there has been an increased focus on swine influenza A virus (swIAV) surveillance.
17 lified the transmission and zoonotic risk of swine influenza A virus (swIAV).
18                                              Swine influenza A virus is an endemic and economically i
19 WIV or virus-vectored vaccines reduces pH1N1 swine influenza A virus shedding following challenge and
20                                              Swine influenza A viruses (IAV) are a major cause of res
21                                              Swine influenza A viruses (swIAVs) can play a crucial ro
22  of pdm/09 H1N1 virus highlights the role of swine influenza A viruses (swIAVs) in generating novel i
23 additional 1,404 whole-genome sequences from swine influenza A viruses collected globally during 1931
24 A viruses of animal origin (such as avian or swine influenza A viruses), which are antigenically and
25 s are evidently more resistant to avian than swine influenza A viruses, mediated in part through fron
26 cific for the detection of human, avian, and swine influenza A viruses.
27 s are higher than those of human and classic swine influenza A viruses.
28 ed to assess persistence of antibody against swine influenza A/H1N1(2009) pandemic influenza, childre
29 am began in January 1976 with an outbreak of swine influenza among trainees at Ft. Dix, New Jersey.
30 rigins of the pandemic virus and the classic swine influenza and (postpandemic) seasonal H1N1 lineage
31 69 ferrets infected with seasonal influenza, swine influenza, and highly pathogenic avian influenza (
32                   Concern that pandemic H1N1 swine influenza could be transmitted by solid organ tran
33  ecobiological association between human and swine influenza could extend to before 1918.
34 is of human ICV (huICV) in comparison to the swine influenza D virus (swIDV) in guinea pigs.
35                       Since its detection in swine, influenza D virus (IDV) has been shown to be pres
36 918, but an anecdotal report suggests that a swine-influenza epizootic might have occurred in England
37 gin reassortant containing human, avian, and swine influenza genes.
38 equence comparison of the variant viruses to swine influenza genomes.
39 A/New Caledonia/20/99 [Ncal99]), a classical swine influenza H1N1 virus isolate (A/Swine/Iowa/15/30 [
40 lowing in vitro infection with 2009 pandemic swine influenza (H1N1/09).
41                                              Swine influenza has been recognised only since 1918, but
42                                          The Swine Influenza Immunization Program began in January 19
43                   Drawing from the ill-fated swine influenza immunization program of 1976, this artic
44  influenza, and diminished lung pathology in swine-influenza-infected piglets.
45 By contrast with the recent documentation of swine influenza, influenza in horses has been well docum
46                                              Swine influenza is a highly contagious zoonotic disease
47                                              Swine influenza is an acute respiratory disease caused b
48 lly poorly transmitted between humans, while swine influenza is better transmitted due to glycan simi
49 orth American swine breeding herds, managing swine influenza is challenging primarily due to the cont
50                                   Control of swine influenza is primarily through the vaccination of
51 2009 virus was derived from well-established swine influenza lineages; however, there is no convincin
52 ity to pandemic H1N1 hemagglutinin after the swine influenza pandemic of 2009 in pooled human polyclo
53 luenza A virus strains, such as the new H1N1 swine influenza, represents a serious threat to global h
54 lCer generates protective immunity against a swine influenza (SI) virus infection when applied as an
55                        In 1976, the national swine influenza vaccination program in the United States
56 drome (GBS) occurred among recipients of the swine influenza vaccine in 1976-1977.
57 e (GBS) following administration of the 1976 swine influenza vaccine led to a heightened focus on GBS
58  data demonstrate the importance of matching swine influenza vaccine seed strains to contemporary cir
59       Vaccination with the A/New Jersey/1976 swine influenza vaccine substantially boosted cross-reac
60 ain-Barre Syndrome (GBS) found with the 1976 swine influenza vaccine, both active surveillance and en
61 ruses tested were antigenically distant from swine influenza vaccine-representative strains, highligh
62 tantially lower than that seen with the 1976 swine influenza vaccine.
63   GBS has also been associated with the 1976 swine-influenza vaccine.
64 were vaccinated with recent seasonal or 1976 swine influenza vaccines.
65 lb09]), with that of the 1918-like classical swine influenza virus (A/swine/Iowa/1930 [IA30]) in the
66                                   In 2009, a swine influenza virus (pH1N1) jumped to humans and sprea
67                                              Swine influenza virus (SIV) can cause respiratory illnes
68                                              Swine influenza virus (SIV) H3N2 with triple reassorted
69 1-F2 protein of triple-reassortant (TR) H3N2 swine influenza virus (SIV) in pigs and turkeys.
70 raction between Mycoplasma hyopneumoniae and swine influenza virus (SIV) in the induction of pneumoni
71 dentifying a student with triple-reassortant swine influenza virus (SIV) infection and pig exposure a
72 ole of the NS1 protein in the virulence of a swine influenza virus (SIV) isolate in pigs by using rev
73            The Eurasian avian-like (EA) H1N1 swine influenza virus (SIV) possesses the capacity to in
74 ation of a so-called triple reassortant (TR) swine influenza virus (SIV).
75                                              Swine influenza virus (SwIV) is one of the important zoo
76               As a positive control, an H3N2 swine influenza virus A was used.
77 y shown to enhance the replication of a 1976 swine influenza virus also significantly improved the re
78  stages of the European avian-like (EA) H1N1 swine influenza virus as it transitioned from avian to s
79                Novel triple-reassortant H3N2 swine influenza virus emerged in 1998 and spread rapidly
80  we examine the innate antiviral response to swine influenza virus in primary and immortalized swine
81 n that infection in humans with the pandemic swine influenza virus induces antibodies with specificit
82                                 Before 1998, swine influenza virus isolates in the United States were
83 recursor strains from the triple-reassortant swine influenza virus lineage, which cause only sporadic
84 , and nonstructural genes being of classical swine influenza virus origin, and the PA and PB2 polymer
85    The recent flu epidemic caused by an H1N1 swine influenza virus presents an opportunity to examine
86 Biosystems 7500 Fast platform, using the CDC swine influenza virus real-time RT-PCR detection panel (
87 in A/New Caledonia/20/1999 and 2009 pandemic swine influenza virus strain A/California/04/2009.
88 rotected completely against lethal avian and swine influenza virus strains in mice, and induced robus
89 to a representative human triple-reassortant swine influenza virus that has circulated in pigs in the
90 ls which recovered from exposure to virulent swine influenza virus were completely resistant to infec
91 th the reconstructed 1918 virus, a 1976 H1N1 swine influenza virus, and a highly pathogenic H5N1 viru
92 CD8(+) T-cell epitopes in NP of human versus swine influenza virus, consistent with the idea that the
93                   Therefore, we chose a H1N1 swine influenza virus, Sw/OH/24366/07 (SwIV), which has
94                             Unlike classical swine influenza virus, TR SIV produces a full-length PB1
95 onstrate here that an engineered reassortant swine influenza virus, with the same gene constellation
96                               We report that swine influenza virus-like substitutions T200A and E227A
97               A new H1N1 triple-reassortant "swine" influenza virus was recently described in individ
98 e its absence from some animal (particularly swine) influenza virus isolates, variable expression in
99                                              Swine influenza viruses (SIV) have been shown to sporadi
100                                              Swine influenza viruses (SIV) naturally infect pigs and
101                           Triple reassortant swine influenza viruses (SIVs) and 2009 pandemic H1N1 (p
102               Since the introduction of H3N2 swine influenza viruses (SIVs) into U.S. swine in 1998,
103                             We identified 34 swine influenza viruses (termed rH3N2p) with the same co
104 logic factors that limit the transmission of swine influenza viruses between humans are unresolved.
105  virus reassortment, as avian, human, and/or swine influenza viruses can infect swine and reassort, a
106  large-scale genomic characterization of 290 swine influenza viruses collected from 14 European count
107                          The results suggest swine influenza viruses containing both a stabilized HA
108 enting the avian-like precursor virus and EA swine influenza viruses from 1979-1983, 1984-1987 and 19
109 ttle known about the host barriers that keep swine influenza viruses from entering the human populati
110 se data highlight the increased diversity of swine influenza viruses in the United States and would i
111 fluenza subtypes by mixing avian, human, and swine influenza viruses is possible.
112                                          For swine influenza viruses isolated in 2009-2016, gamma-cla
113        Due to their attenuation, NS1-mutated swine influenza viruses might have a great potential as
114                   Critically, both human and swine influenza viruses replicated in the immortalized c
115 all proposed to have been caused by avian or swine influenza viruses that acquired virulence factors
116 e epitopes in parallel lineages of human and swine influenza viruses that have been diverging since r
117         Here we use comparisons of human and swine influenza viruses to rigorously demonstrate that h
118 y (typically found in avian and classic H1N1 swine influenza viruses), conferring binding to human- a
119 uman H1N1 influenza A virus strains, several swine influenza viruses, and influenza B viruses but wer
120 uenza viruses, unlike other human, avian and swine influenza viruses, are resistant to the antiviral
121 nes can be recombined from human, avian, and swine influenza viruses, leading to triple reassortants.
122     However, when transferred into avian and swine influenza viruses, only partial ts and attenuation
123 ing a panel of 28 distinct human, avian, and swine influenza viruses, we found that only a small subs
124 ses--containing genes from avian, human, and swine influenza viruses--emerged and became enzootic amo
125 tinin receptor-binding specificity of the EA swine influenza viruses-that is, from recognition of bot
126 modon hispidus) are susceptible to avian and swine influenza viruses.
127 nd might reassort with currently circulating swine influenza viruses.
128 l cells which is characteristic for virulent swine influenza viruses.
129 es and antigenically distinct from reference swine influenza viruses.
130  understanding of the antigenic diversity of swine influenza will facilitate a rational approach for

 
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