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1 hospitalized transplant recipients with 2009 H1N1 influenza virus.
2 ed into recombinant A/Puerto Rico/8/34 (PR8) H1N1 influenza virus.
3  than did pigs infected with wild-type human H1N1 influenza virus.
4 terpene with remarkable activity against the H1N1 influenza virus.
5 ral lung titers, following challenge with an H1N1 influenza virus.
6 IV (mean of 64 days), were challenged with A/H1N1 influenza virus.
7 tein 1, and polymerase basic protein 1 of an H1N1 influenza virus.
8 ate 100% survival from lethal challenge with H1N1 influenza virus.
9 ram) anti-influenza antibodies binding to an H1N1 influenza virus.
10 ere introduced into the genome of a seasonal H1N1 influenza virus.
11 e from a lethal challenge with 2009 pandemic H1N1 influenza virus.
12 ses and protective efficacy against pandemic H1N1 influenza virus.
13 he first reported cases of the pandemic 2009/H1N1 influenza virus.
14 cing infection with high viral loads of 2009 H1N1 influenza virus.
15 iruses and to specifically identify the 2009 H1N1 influenza virus.
16 oss-protection against the swine-origin 2009 H1N1 influenza virus.
17 otect against the pandemic swine-origin 2009 H1N1 influenza virus.
18 nt recipients; 4 were confirmed to have 2009 H1N1 influenza virus.
19        Testing was with nebulized A/PR/8/34 (H1N1) influenza virus.
20 inhibition (HAI) activity against a panel of H1N1 influenza viruses.
21 f historical seasonal-like and pandemic-like H1N1 influenza viruses.
22 cted with either 1918 or 2009 human pandemic H1N1 influenza viruses.
23 ing a potent neutralization activity against H1N1 influenza viruses.
24 ss2, in knockout mice inhibits the spread of H1N1 influenza viruses.
25 nt as therapeutic agents against circulating H1N1 influenza viruses.
26 infection with two pandemic and two seasonal H1N1 influenza viruses.
27 tion H274Y in the neuraminidase (NA) gene of H1N1 influenza viruses.
28 ough the host was never exposed to the novel H1N1 influenza viruses.
29 urred in the HA of naturally occurring human H1N1 influenza viruses.
30 e from lethal challenges with either H5N1 or H1N1 influenza viruses.
31 resulted in a decrease in the replication of H1N1 influenza viruses.
32  by a virus very similar to present swine (A/H1N1) influenza viruses.
33 o confer protection against a lethal dose of H1N1 influenza virus A/Puerto Rico 8/34 (PR8).
34 04 (VN1203), and the NA of the mouse-adapted H1N1 influenza virus A/Puerto Rico/8/34 (PR8) in the VSV
35 of cell death is a distinguishing feature of H1N1 influenza virus A/Puerto Rico/8/34 protein PB1-F2.
36 s were protected from challenge with a novel H1N1 influenza virus (A/California/07/2009), and these f
37 r M-Tri-DAP and subsequently challenged with H1N1 influenza virus (A/England/195/2009).
38 vector encoding the hemagglutinin (HA) of an H1N1 influenza virus (A/Swine/Indiana/1726/88) to porcin
39 structure in complex with HA from a pandemic H1N1 influenza virus, A/South Carolina/1/1918(H1N1), rev
40 eplaced with genes from a contemporary human H1N1 influenza virus, A/Texas/36/91 (Tx/91), were genera
41 nversion, ferrets were challenged with novel H1N1 influenza virus and assessed for viral titers in th
42 omolgus macaques with highly pathogenic 1918 H1N1 influenza virus and assessed pathogenesis and disea
43 ted to understand better the pathogenesis of H1N1 influenza virus and associated host mucosal immune
44 with escalating concerns regarding the novel H1N1 influenza virus and its recently approved vaccine,
45  mechanism underlying broad immunity against H1N1 influenza viruses and identifies a conserved epitop
46 , Muc5ac-Tg animals were challenged with PR8/H1N1 influenza viruses and showed significant decreases
47                Exposure to multiple seasonal H1N1 influenza viruses, and not to any single H1N1 influ
48 natural history and transmission of the 2009 H1N1 influenza virus appear to be similar to those of pr
49              In early 2009, a novel pandemic H1N1 influenza virus appeared, but it has not exhibited
50                                              H1N1 influenza viruses are responsible for both seasonal
51 ferrets with antigenically distinct seasonal H1N1 influenza viruses boosts the antibody responses dir
52               However, oseltamivir-resistant H1N1 influenza viruses carrying the H275Y NA mutation sp
53                        Oseltamivir-resistant H1N1 influenza viruses carrying the H275Y neuraminidase
54                                           An H1N1 influenza virus caused a pandemic in 2009, and desc
55 ast to seasonal influenza H1N1 virus, 2009 A(H1N1) influenza viruses caused increased morbidity, repl
56 ce from homologous and heterologous H3N2 and H1N1 influenza virus challenge.
57 100% in vivo protection efficacy against the H1N1 influenza virus challenge.
58 ity and improved protection against the 2009 H1N1 influenza virus, compared with subcutaneous injecti
59 e, the X-181 strain of the 2009 new pandemic H1N1 influenza virus, derived from the A/California/07/2
60 e hemagglutinin and nucleoprotein genes from H1N1 influenza virus developed serum anti-H1 immunoglobu
61 nstrate that memory CD4 T cells specific for H1N1 influenza virus directed protective responses to in
62 reover, sequential infection of ferrets with H1N1 influenza viruses elicited an Igkappa-biased Ab res
63 expressing NA from avian (H5N1) or pandemic (H1N1) influenza virus, elicited NA-specific antibody and
64 1N1 influenza viruses, and not to any single H1N1 influenza virus, elicits a breadth of antibodies th
65                                      A novel H1N1 influenza virus emerged in 2009 (pH1N1) to become t
66                             In 2009, a novel H1N1 influenza virus emerged in humans, causing a global
67 The rapid dissemination of the 2009 pandemic H1N1 influenza virus emphasizes the need for universal i
68                             Here, we used an H1N1 influenza virus encoding a fluorescent reporter gen
69 is report, we show that recombinant H5N1 and H1N1 influenza viruses encoding a truncated NS1 protein
70  evidence supporting the hypothesis that the H1N1 influenza virus entered the human population just p
71                                   The 2009 A(H1N1) influenza viruses exhibited less efficient respira
72                     Primary infection with s-H1N1 influenza virus followed by a dose of p-LAIV result
73 een preferentially eliminated from classical H1N1 influenza virus genomes during virus evolution in h
74  all challenge viruses, including a relevant H1N1 influenza virus group 1 strain, with minimal weight
75 , the avian-derived PB2 of the 2009 pandemic H1N1 influenza virus has 271A.
76           The emergence of the pandemic 2009 H1N1 influenza virus has become a world-wide health conc
77                            Swine origin 2009 H1N1 influenza virus has spread globally to cause the fi
78 es that elicit protective antibodies against H1N1 influenza viruses have been developed.
79                               Drug-resistant H1N1 influenza viruses have dominated the 2009 flu seaso
80                Thus, our data show that 2009 H1N1 influenza viruses have evolved after pandemic onset
81 re is increasing evidence that 2009 pandemic H1N1 influenza viruses have evolved after pandemic onset
82 tration was associated with lower odds for A/H1N1 influenza virus illness, indicating its potential a
83 tration was associated with lower odds for A/H1N1 influenza virus illness, indicating its potential a
84 fection with pandemic-like and seasonal-like H1N1 influenza viruses.IMPORTANCE There is a great need
85 g the emergence and global spread of a novel H1N1 influenza virus in 2009, two A(H1N1)pdm/09 influenz
86 en associated with the 2009-2010 pandemic of H1N1 influenza virus in China and with mass vaccination
87             The transmissibility of the 2009 H1N1 influenza virus in households is lower than that se
88 ve relevance to pathogenesis of the pandemic H1N1 influenza virus in humans; thus, pigs may serve as
89 ne from an H5N1 virus rescued replication of H1N1 influenza virus in macrophages.
90 h displayed an EC50 value of 2.1 muM against H1N1 influenza virus in MDCK cells.
91                  We show that infection with H1N1 influenza virus in mice that lack B and T cells (Re
92                       The spread of the 2009 H1N1 influenza virus in the population worldwide, in add
93                        We show that pandemic H1N1 influenza virus in which the hemagglutinin signal s
94 essential for the spread and pathogenesis of H1N1 influenza viruses in mice.
95 mmalian (swine H1N1, human H1N1 and pandemic H1N1) influenza viruses in PAM.
96 hile the seroprevalence of seasonal H3N2 and H1N1 influenza viruses increased with the decline of amb
97             Accordingly, SARS-CoV-2, but not H1N1 influenza virus, increases levels of brain IL-1beta
98 kines were also seen in either SARS-CoV-2 or H1N1 influenza virus-infected mice, which were treated a
99 ibution and severity of pneumonia after 2009 H1N1 influenza virus infection in newly weaned, adult, a
100 The estimated rate of admission for pandemic H1N1 influenza virus infection in pregnant women during
101 dation to promptly treat pregnant women with H1N1 influenza virus infection with anti-influenza drugs
102 nstrated lung regeneration in mice following H1N1 influenza virus infection, and linked distal airway
103 lated form as new therapeutic agents against H1N1 influenza virus infection.
104 protects ferrets against aerosol-transmitted H1N1 influenza virus infection.
105 st TLR-triggered immune response and cleared H1N1 influenza virus infection.
106 revention of disease and control of pandemic H1N1 influenza virus infection.
107 ) to mediate protection against swine-origin H1N1 influenza virus infection.
108    A remarkable feature of the 2009 pandemic H1N1 influenza virus is its efficient transmissibility i
109 ily accelerated clearance of a 2009 pandemic H1N1 influenza virus isolate in an antibody-dependent ma
110 based vaccine for both seasonal and pandemic H1N1 influenza virus isolates.
111                                     The 2009 H1N1 influenza virus outbreak is the first pandemic of t
112 ith heterologous strains, including the 2009 H1N1 influenza virus pandemic strain.
113                                     The 1918 H1N1 influenza virus pandemic was the most severe of the
114 omestic pigs infected with the 2009 pandemic H1N1 influenza virus (pH1N1) have been detected worldwid
115  death from infection with the 2009 pandemic H1N1 influenza virus (pH1N1).
116 ss-species transmission of the 2009 pandemic H1N1 influenza virus (pH1N1).
117    Preexisting immunity to the 2009 pandemic H1N1 influenza virus prevented severe H5N1 disease and r
118       Subsequent human infections with novel H1N1 influenza viruses prompted an investigation of the
119 eal that first exposure to the 2009 pandemic H1N1 influenza virus recalls memory B cells that are spe
120 damage and high lethality caused by the 1918 H1N1 influenza virus remains largely unknown.
121 regulated in the lungs of patients with 2009 H1N1 influenza virus, respiratory syncytial virus, or pa
122 major concern about the ongoing swine-origin H1N1 influenza virus (S-OIV) outbreak is that the virus
123 to elicit antibody responses that neutralize H1N1 influenza viruses spanning over 90 years.
124 luenza A and B viruses, including a pandemic H1N1 influenza virus strain, a highly pathogenic H5N1 av
125 ed to the disappearance of existing seasonal H1N1 influenza virus strains.
126         Pigs infected with recombinant human H1N1 influenza virus that carried the H5N1 NS gene exper
127  we determined the ability of representative H1N1 influenza viruses that circulated in the human popu
128 h seasonal H1N1 and triple-reassortant swine H1N1 influenza viruses that have circulated among North
129                                          For H1N1 influenza viruses, the mouse-adapted A/WSN/33 strai
130 humans caused by a novel swine-origin 2009 A(H1N1) influenza virus underscore the need to better unde
131                                     The 2009 H1N1 influenza virus was first identified in April 2009
132 ted with highly pathogenic H5N1 and seasonal H1N1 influenza viruses was evaluated using mass spectrom
133                   Transmission of the 2009 A(H1N1) influenza viruses was further corroborated by char
134                                              H1N1 influenza viruses were responsible for the 1918 pan
135 ortment between H3N2 human and classic swine H1N1 influenza viruses, while the others arose from reas
136 t and infectious HIV, hepatitis C virus, and H1N1 influenza virus, whole-genome gene expression analy
137 in ferrets infected with any single seasonal H1N1 influenza viruses, with limited protection to chall
138 oled and tested for the presence of the 2009 H1N1 influenza virus without a reduction in sensitivity.

 
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