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1 tiviral and clinical effects in experimental human influenza.
2 n either preventing or treating experimental human influenza.
3 epitope on M2e, was explored in experimental human influenza.
4 emporally and geographically to epidemics of human influenza.
5 plosive epidemic (or pandemic recurrence) of human influenza.
6 of the hemagglutinin of approximately 13,000 human influenza A (H3N2) viruses from six continents dur
7 eviously found in the highly pathogenic (HP) human influenza A (H7N9) [IAV(H7N9)] strains.
8                                              Human influenza A (subtype H3N2) is characterized geneti
9  are susceptible to infection with avian and human influenza A and B viruses and have been widely use
10                                              Human influenza A and B viruses infected cells from geog
11 rior adaptation that is usually required for human influenza A H1N1 viruses.
12 e fully susceptible to infection with either human influenza A or B viruses.
13 the HA1 domain of the hemagglutinin genes of human influenza A subtype H3 appear to be under positive
14                                              Human influenza A virus (IAV) vaccination is limited by
15 /20/99) or an H3 serotype (A/Panama/2007/99) human influenza A virus and then used these constructs a
16                An especially novel aspect of human influenza A virus binding is its ability to equiva
17                                          The human influenza A virus continues to thrive even among p
18             Although the surface proteins of human influenza A virus evolve rapidly and continually p
19      Here we investigated the replication of human influenza A virus in bat cell lines and the barrie
20  its recognition by the immune system during human influenza A virus infection.
21  the possible roles of anti-M2 antibodies in human influenza A virus infection.
22 y reference strain derived from the earliest human influenza A virus isolate, WS/33.
23 this residue is not conserved in a number of human influenza A virus isolates.
24 n influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, w
25 that phosphorylation of the NS1 protein of a human influenza A virus occurs not only at the threonine
26     To determine the role of MxA in blocking human influenza A virus replication in primate cells, we
27                   Deep sequencing of adapted human influenza A virus revealed a mutation in the PA po
28 ly, found in the NS1A proteins of almost all human influenza A virus strains.
29 ial cells, the primary cell type infected by human influenza A virus strains.
30 y phosphorylation of the NS1 protein of this human influenza A virus that regulates its replication i
31                               We showed that human influenza A virus uses canonical sialic acid recep
32 ts of sequencing 209 complete genomes of the human influenza A virus, encompassing a total of 2,821,1
33 801) elicit robust CTL responses against any human influenza A virus, including H7N9, whereas ethnici
34 ne the extent of homologous recombination in human influenza A virus, we assembled a data set of 13,8
35 s only a very minor role in the evolution of human influenza A virus.
36 mples of such viruses include three pandemic human influenza A viruses and canine parvovirus in dogs.
37                         The NS1A proteins of human influenza A viruses bind CPSF30, a cellular factor
38                           The NS1 protein of human influenza A viruses binds the 30-kDa subunit of th
39 it of the RNA polymerase complex of seasonal human influenza A viruses has been shown to localize to
40         Our data suggest that replication of human influenza A viruses in a nonnative host drives the
41 sing the pandemic risk posed by specific non-human influenza A viruses is an important goal in public
42 esults suggest that the currently prevailing human influenza A viruses might have lost their ability
43                                              Human influenza A viruses preferentially bind alpha2,6-l
44  as one mechanism for the emergence of novel human influenza A viruses.
45 the relative virulence of selected avian and human influenza A viruses.
46 cid residues that are highly conserved among human influenza A viruses.
47 e and replaced the HA gene of the prevailing human influenza A viruses.
48 otoxicity was demonstrated against avian and human influenza A viruses.
49 ," is virucidal for H1 hemagglutinin-bearing human influenza A viruses.
50 was similar to that of a primary response to human influenza A viruses; serum neutralizing antibody w
51 led PREDAC-H3, for antigenic surveillance of human influenza A(H3N2) virus based on the sequence of s
52        We have studied the HA1 domain of 254 human influenza A(H3N2) virus genes for clues that might
53  thus assisting in antigenic surveillance of human influenza A(H3N2) virus.
54   Our results indicate that the evolution of human influenza A(H3N2) viruses since 1968 has produced
55 imated the incubation period distribution of human influenza A(H7N9) infections using exposure data a
56    Studies reporting serological evidence of human influenza A(H9N2) infection among avian-exposed po
57      We further show that vaccinia virus and human influenza A, B, and C viruses each encode an essen
58  of cytotoxic T lymphocyte escape mutants in human influenza A.
59 sampling bias affect evolutionary studies of human influenza A.
60                                              Human influenza A/B viruses are unusual in preferring al
61               Hemagglutinin sequences of 146 human influenza A/H3N2 strains identified in respiratory
62                                 The seasonal human influenza A/H3N2 virus undergoes rapid evolution,
63        Here, we demonstrate that recombinant human influenza A/H3N2 viruses without and with oseltami
64 us vaccine produced by truncating NS1 in the human influenza A/Texas/36/91 (H1N1) virus with that of
65                      The NS1A protein of the human influenza A/Udorn/72 (Ud) virus inhibits the produ
66 ition to mass vaccination strategies against human influenza, and for the management of antigenically
67               In 1997, 18 confirmed cases of human influenza arising from multiple independent transm
68                                     Although human influenza B virus (IBV) is a significant human pat
69  the corresponding dsRNA binding domain from human influenza B virus NS1B-(15-93).
70 ions we inferred the phylogenetic history of human influenza B virus using complete genome sequences
71 h less depleted than suggested by a model of human influenza based only on virus-shedding data.
72   Viruses with approximately 50% homology to human influenza C virus (ICV) have recently been isolate
73 revious studies support an increased risk of human influenza cases among individuals with swine conta
74 athological analysis of autopsy samples from human influenza cases from 1918 revealed significant dam
75 on sequencing (NGS) samples generated from a human influenza challenge study wherein 17 healthy subje
76 nship between the degree of inflammation and human influenza disease progression are scarce.
77 ouse experimental model systems for studying human influenza disease.
78  opportunities for more effective control of human influenza epidemics and pandemics by inactivated i
79  model through clinically-relevant, seasonal human influenza examples.
80 ) with a genetically reconstructed strain of human influenza H1N1 A/Texas/36/91 virus and hypothesize
81 key/Turkey/1/05) and a moderately pathogenic human influenza H1N1 virus (A/USSR/77), but there were c
82                These results indicate that a human influenza H1N1 virus possessing the 1918 HA and NA
83            In stark contrast to contemporary human influenza H1N1 viruses, the 1918 pandemic virus ha
84 hly homologous to those of highly pathogenic human influenza H5N1 viruses, suggesting that a W312-lik
85 tibodies, but the precise role of T cells in human influenza immunity is uncertain.
86 ons of these results for vaccination against human influenza infection are discussed.
87   Reports of the use of hyperimmune serum in human influenza infection are sporadic and studies in an
88 more pathways relevant to immune-response to human influenza infection than the competing approaches.
89 dered the most reliable animal surrogate for human influenza infection, the newly engineered H5N1 str
90 ge-scale time-course gene expression data on human influenza infection, we demonstrate that our metho
91                                              Human influenza infections display a strongly seasonal p
92 ts, creating a clinical infection similar to human influenza infections.
93                                              Human influenza is a highly contagious acute respiratory
94                                              Human influenza is a seasonal disease associated with si
95                       A more cogent model of human influenza is the ferret.
96 accine encoding hemagglutinin from the index human influenza isolate A/HK/156/97 provides immunity ag
97                       The threat of pandemic human influenza looms as we survey the ongoing avian inf
98  especially critical determinant of observed human influenza mortality, even after controlling for te
99 ng normal or variant antigenic peptides from human influenza nucleoprotein.
100                                              Human influenza occurs annually in most temperate climat
101 n Hong Kong raises the possibility of future human influenza outbreaks.
102  raised worldwide concern about an impending human influenza pandemic similar to the notorious H1N1 S
103                        Will there be another human influenza pandemic?
104            We find that the four most recent human influenza pandemics (1918, 1957, 1968, and 2009),
105 h airborne transmissibility, suggesting that human influenza pandemics caused by these influenza A(H5
106  1957 (H2N2 subtype) and 1968 (H3N2 subtype) human influenza pandemics.
107 t the clinical relevance of this protease in human influenza pathogenesis.
108 ent in ferrets, the primary animal model for human influenza pathogenesis.
109     In late 2011 and early 2012, 13 cases of human influenza resulted from infection with a novel tri
110 (H1N1), a mouse-adapted virus derived from a human influenza strain first isolated in 1933.
111 and variability in transmissibility of novel human influenza strains as they emerge is a key public h
112  of identified epitopes among avian H5N1 and human influenza strains.
113 d discovered a peptide that destroys diverse human influenza strains.
114 d on antigenic distance and from a published human influenza study.
115                               In the case of human influenza, such potential benefits of mass vaccina
116  because the disease state resembles that of human influenza, these animals have been widely used as
117                  We used the ferret model of human influenza to systematically investigate viral inte
118                              Direct avian-to-human influenza transmission was unknown before 1997.
119  The ectodomain of matrix protein 2 (M2e) of human influenza type A virus strains has remained remark
120  design of optimal immunization regimens for human influenza vaccines, especially for influenza-naive
121 nvestigated the role of maternal exposure to human influenza virus [HI] in C57BL/6 mice on day 9 of p
122 d the aerosol transmission efficiencies of 2 human influenza virus A strains and found that A/Panama/
123  hominoids, the hemagglutinin (HA) gene from human influenza virus A, and HIV-1 env, vif, and pol gen
124  very high (>98%) nucleotide homology to the human influenza virus A/Hong Kong/156/97 (H5N1) in the s
125 ge and with geometric mean antibody titer to human influenza virus antigens.
126 C-terminal truncations in the NS1 protein of human influenza virus are sufficient to make the virus a
127                                     Seasonal human influenza virus continues to cause morbidity and m
128 e polymerase protein sequences from the 1918 human influenza virus differ from avian consensus sequen
129 uenza viruses to rigorously demonstrate that human influenza virus evolves under pressure to fix muta
130  but this effect is less well understood for human influenza virus HA proteins that lack polybasic cl
131  considered the 'gold standard' for modeling human influenza virus infection and transmission.
132 ng IFITM3 proteins were involved in blocking human influenza virus infection in endothelial cells.
133 support the premise that a barrier exists to human influenza virus infection in pigs, which may limit
134                                 We show that human influenza virus infection is blocked during the ea
135     The "gold standard" for serodiagnosis of human influenza virus infection is the detection of sero
136                To test the role of IFITM3 in human influenza virus infection, we assessed the IFITM3
137 spiratory death after mouse parainfluenza or human influenza virus infection.
138 anscript changes in blood during symptomatic human influenza virus infection.
139 e of novel pandemic H1N1 as well as seasonal human influenza virus infections in domestic cats in Ohi
140                  The serial interval (SI) of human influenza virus infections is often described by a
141 apply this method to an existing data set of human influenza virus infections, showing that transmiss
142 A/NA can play important roles in controlling human influenza virus infectivity in pigs.
143 e dynamics and control, but its relevance to human influenza virus is still unclear.
144 t only markers which are highly preserved in human influenza virus isolates over time.
145  We have previously shown that a recombinant human influenza virus lacking the NS1 gene (delNS1) coul
146 virus with 3 A(H1N1)pdm09 genes and a recent human influenza virus N2 gene was transmitted most effic
147 re is clear selection from CD8(+) T cells in human influenza virus NP and illustrates how comparative
148  show that epitope-altering substitutions in human influenza virus NP are enriched on the trunk versu
149                             However, even in human influenza virus NP, sites in T-cell epitopes evolv
150 ed the activities of polymerases of avian or human influenza virus origin in pig, human, and avian ce
151 aminidase, and PB1 polymerase genes being of human influenza virus origin, the nucleoprotein, matrix,
152 n early warning of the emergence of the next human influenza virus pandemic.
153  using both the 2009 H1N1 ID kit and the CDC human influenza virus real-time reverse transcription-PC
154 tently differentiate the 1918 and subsequent human influenza virus sequences from avian virus sequenc
155 elated either to avian influenza virus or to human influenza virus strains from Asia from the 1960s,
156  type, subtype, and determine the lineage of human influenza virus strains through the detection of o
157 human endothelial cells limit replication of human influenza virus strains, whereas avian influenza v
158 escribing the phylodynamics of interpandemic human influenza virus subtype A(H3N2).
159 of the RBS naturally varies across avian and human influenza virus subtypes and is also evolvable.
160         The highest titers were observed for human influenza virus subtypes.
161  residues important for NS1 functions and in human influenza virus surveillance to assess mutations a
162 (Mph) demonstrated greater susceptibility to human influenza virus than monocytes, with the majority
163 r transgenic mouse (2D2) and a mouse-adapted human influenza virus to test the hypothesis that upper-
164 mong sites are used to analyze a data set of human influenza virus type A hemagglutinin (HA) genes.
165          The preparation of live, attenuated human influenza virus vaccines and of large quantities o
166 e (both BALB/c and C57BL/6 strains) with the human influenza virus yields offspring that display high
167 ne from A/Texas/36/91 (a seasonal isolate of human influenza virus), as well as the host response to
168 re based on maternal gestational exposure to human influenza virus, the viral mimic polyriboinosinic-
169 a hemagglutinin and neuraminidase from a non-human influenza virus, we assessed which of the three ce
170           Contrary to previous findings with human influenza virus, we found that in the case of equi
171 these vesicles have a neutralizing effect on human influenza virus, which is known to bind sialic aci
172 diversity in recently circulating strains of human influenza virus.
173  a descendant of the 1918 pandemic strain of human influenza virus.
174  are naturally susceptible to infection with human influenza viruses and because the disease state re
175 operties that more closely resemble those of human influenza viruses and have the potential to spread
176 y to assess the risks posed to humans by non-human influenza viruses and lead to improved pandemic pr
177                                              Human influenza viruses and Parvovirus Minute Viruses of
178 ed at least three distinct H3 molecules from human influenza viruses and thus form three distinct phy
179 erally replicate at higher temperatures than human influenza viruses and, although they shared the sa
180                                              Human influenza viruses are proposed to recognize sialic
181                                 For example, human influenza viruses do not replicate in duck intesti
182        CIV evolves at a lower rate than H3N2 human influenza viruses do, and viral phylogenies exhibi
183                 The hemagglutinin (HA) of H3 human influenza viruses does not support viral replicati
184 n in vivo, we have generated two recombinant human influenza viruses encoding either mitochondrial or
185 inic acid alpha3 (NeuAcalpha3) sugars, while human influenza viruses exhibit a preference for NeuAcal
186 cid, we identified markers that discriminate human influenza viruses from avian influenza viruses.
187  Hemagglutinins (HA's) from duck, swine, and human influenza viruses have previously been shown to pr
188                Our studies with contemporary human influenza viruses identified escape mutants before
189 irus is compatible for genetic exchange with human influenza viruses in human cells, suggesting the p
190                       Although we found that human influenza viruses infected both ciliated and nonci
191 uried surface of the complex have mutated in human influenza viruses isolated after 1998, confirming
192  In particular, the PB2 proteins of seasonal human influenza viruses localize to the mitochondria whi
193  clear whether prior exposure to circulating human influenza viruses or influenza vaccination confers
194  H5) influenza viruses, we observed that the human influenza viruses primarily infected ciliated cell
195 termines resistance of seasonal and pandemic human influenza viruses to Mx, while avian isolates reta
196 genes via reassortment and the adaptation of human influenza viruses to new swine hosts.
197                                    In HULEC, human influenza viruses were capable of binding to host
198 assays of viral traits to identify those non-human influenza viruses with the greatest risk of evolvi
199 ing specificity with Asp (typically found in human influenza viruses) and Gly (typically found in avi
200 se they possess receptors for both avian and human influenza viruses, and emergence may occur in sout
201 antiviral activity against avian, swine, and human influenza viruses, and the antiviral effect of TNF
202 e susceptible to infection by both avian and human influenza viruses, and this feature is thought to
203 H3 and N1 and N2 antigens have been found in human influenza viruses, but virologic history is too br
204 e-based assays for susceptibility testing of human influenza viruses, detection of DeltaRNA segments
205                                         Like human influenza viruses, EIV H3N8 caused a transcontinen
206 triple reassortant between avian, swine, and human influenza viruses, highlighting the importance of
207  endothelium possesses intrinsic immunity to human influenza viruses, in part due to the constitutive
208 t guinea pigs can be infected with avian and human influenza viruses, resulting in high titers of vir
209 an intermediate host in the emergence of new human influenza viruses, there is still little known abo
210 st studies have focused on NAI-resistance in human influenza viruses, we investigated the molecular c
211 r pigs as possible adaptation hosts of novel human influenza viruses.
212 ot cross-react with HAs of more contemporary human influenza viruses.
213 ceptibility to infection with both avian and human influenza viruses.
214 binding molecules preferred by the avian and human influenza viruses.
215  infection, a specificity also described for human influenza viruses.
216 ely resistant to experimental infection with human Influenza viruses.
217 e that had been previously immunized against human influenza viruses.
218 e spatio-temporal incidence and evolution of human influenza viruses.
219  pH for hemagglutinin activation, similar to human influenza viruses.
220 se of their susceptibility to both avian and human influenza viruses.
221  infection, replication, and spread of seven human influenza viruses.
222 els are substantially different in swine and human influenza viruses.

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