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1  confirmed by analyzing different strains of influenza A virus.
2 the wild-type and V27A mutant M2 channels of influenza A virus.
3  important for the replicative efficiency of influenza A virus.
4  a kind of glycoprotein that is found on the influenza A virus.
5  (MVBs) and the endocytic host cell entry of influenza A virus.
6 e open reading frame in PB1 segments of most influenza A virus.
7  redundant bystander during coinfection with influenza A virus.
8 ted to affect the temperature sensitivity of influenza A viruses.
9 ard ducks, the natural host and reservoir of influenza A viruses.
10  assessment of the pandemic risk of zoonotic influenza A viruses.
11 rapeutic potential of 81.39a against diverse influenza A viruses.
12  with pandemic H1N1 (2009) and seasonal H1N1 influenza A viruses.
13 of 81.39a against both seasonal and emerging influenza A viruses.
14 virucidal for H1 hemagglutinin-bearing human influenza A viruses.
15 f segment 8 (NS) circulate in nonchiropteran influenza A viruses.
16 zing diverse subtypes of group 1 and group 2 influenza A viruses.
17 pacts multiple steps in viral replication of influenza A viruses.
18  basic 2 (PB2) and the nucleoprotein (NP) of influenza A viruses.
19 r insights into the replication mechanism of influenza A viruses.
20 le in the defense of mammalian cells against influenza A viruses.
21 the Aries Flu A/B & RSV assay were 98.1% for influenza A virus, 98.0% for influenza B virus, and 97.7
22            The M2-S31N proton channel of the influenza A virus (A/M2) is one of the validated and mos
23 ion and its downstream effects responding to influenza A virus (A/WSN/33 [H1N1]), tumor necrosis fact
24 e estimated the effective population size of influenza A virus across donor-recipient pairs to be app
25 a new lineage in the human population, avian influenza A viruses (AIV) must overcome the intracellula
26                      Subtype H7 avian-origin influenza A viruses (AIVs) have caused at least 500 conf
27                           Reassortment among influenza A viruses allows viruses to expand their host
28 In addition to the continuous circulation of influenza A viruses among various host species, cross-sp
29 cted in universal viral transport medium (80 influenza A virus and 16 influenza B virus positive) fro
30 nsitivities of the Alere test were 71.3% for influenza A virus and 93.3% for influenza B virus, with
31  enhances the susceptibility to infection by influenza A virus and West Nile virus.
32 Ab 3I14 binds and neutralizes groups 1 and 2 influenza A viruses and protects mice from lethal challe
33 sisting of globular head domains from exotic influenza A viruses and stalk domains from influenza B v
34 is one of the major surface glycoproteins of influenza A viruses and the target for the influenza dru
35 ral activities against currently circulating influenza A viruses and their genetic barrier to drug re
36                   The NS1 protein encoded by influenza A virus antagonizes the interferon response th
37  Although vaccines confer protection against influenza A viruses, antiviral treatment becomes the fir
38 the polymerase complex (PB1, PB2, and PA) of influenza A virus are necessary for viral adaptation to
39 of the influenza virus RNA genome.IMPORTANCE Influenza A viruses are a major global health threat, no
40     These findings indicate that LP avian H7 influenza A viruses are able to infect and cause disease
41                                              Influenza A viruses are constantly changing.
42                                              Influenza A viruses are known to primarily replicate in
43                                              Influenza A viruses are major pathogens for humans, dome
44                                              Influenza A viruses are major pathogens for humans, dome
45                  Human infections with novel influenza A viruses are of global public health concern,
46 Segment reassortment and base mutagenesis of influenza A viruses are the primary routes to the rapid
47                                   H7 subtype influenza A viruses are widely distributed and have been
48                 Low-pathogenic (LP) avian H7 influenza A viruses are widely distributed in the avian
49  on the virion surface, is important in both influenza A virus assembly and entry.
50 been previously identified to play a role in influenza A virus assembly were found to complement the
51 moprophylaxis of human infections with novel influenza A viruses associated with severe human illness
52 id (BALF) from a non-lethal mouse model with influenza A virus at 0, 6, 10, 14, 21 and 28 days post i
53                          Unlike conventional influenza A viruses, bat influenza A-like viruses starte
54 K II cells; however, similar to conventional influenza A viruses, bat influenza A-like viruses were r
55                                              Influenza A viruses bear an eight-segmented single-stran
56 ons probably need to be acquired by emerging influenza A viruses before they can spread in the human
57          The NS1 protein from all strains of influenza A virus binds TRIM25, although not all virus s
58                        The data suggest that influenza A virus budding and genome incorporation can o
59 sistant to highly pathogenic avian H5 and H7 influenza A viruses, but were almost as susceptible to i
60  which exerts antiviral activity against the influenza A virus by inhibiting proton conductance of th
61                                              Influenza A viruses can also cause sporadic infections o
62                     Zoonotic transmission of influenza A viruses can give rise to devastating pandemi
63                                              Influenza A viruses can replicate in the olfactory mucos
64                                              Influenza A virus causes pandemics and annual epidemics
65 able of conferring protection in a stringent influenza A virus challenge.
66 both seasons in which the pandemic 2009 H1N1 influenza A virus circulated, ILI peaked earlier in coun
67 o date, transmission models have depended on influenza A virus coinfection, which greatly enhances pn
68 inflammatory immune response to 2 strains of influenza A virus, compared with nonpregnant women, char
69                      NPs from all strains of influenza A viruses contain two nuclear localization sig
70 Antibodies capable of neutralizing divergent influenza A viruses could form the basis of a universal
71 ng with the generation of and maintenance of influenza A virus diversity in exhibition swine, present
72 tion of specific peptides from vaccinia- and influenza A virus-encoded proteins.
73 discuss the implications of reassortment for influenza A virus evolution, including its classically r
74 pression, demonstrating that some strains of influenza A virus express truncated forms of the NS1 pro
75                                              Influenza A viruses express PA-X proteins to suppress gl
76                                   A panel of influenza A viruses expressing chimeric hemagglutinins (
77               A major factor that determines influenza A virus fitness and therefore transmissibility
78              First, frequent introduction of influenza A viruses from commercial swine populations pr
79                                              Influenza A virus gene segment 7 encodes two proteins: t
80 o MHC class I Ag presentation, we engineered influenza A virus gene segment 7 to encode the model H-2
81                                              Influenza A viruses generally mediate binding to cell su
82 acid receptors.IMPORTANCE The interaction of influenza A virus glycoproteins with cell surface recept
83   H15 is the other member of the subgroup of influenza A virus group 2 hemagglutinins (HAs) that also
84 n.Broadly reactive antibodies that recognize influenza A virus HA can be protective, but the mechanis
85 ffinity relationship for interactions of the Influenza A virus HA with bivalent displays of the natur
86                                              Influenza A virus haemagglutinin conformational change d
87 al replication, the M2 proton channel of the influenza A virus has been the focus of many studies.
88 the RNA polymerase complex of seasonal human influenza A viruses has been shown to localize to the mi
89 aminidase (NA) for the intestinal tropism of influenza A viruses has been unclear.
90                                              Influenza A viruses have caused a number of global pande
91                                              Influenza A virus hemagglutinin (HA) initiates viral ent
92 chy to the five major antigenic sites in the influenza A virus hemagglutinin globular domain.
93 n antiviral response, whereas infection with influenza A virus, herpes simplex virus 1, or cytomegalo
94 serve as the principal natural reservoir for influenza A virus; however, the key properties of NA for
95                                              Influenza A virus (IAV) and influenza B virus (IBV) caus
96 the response to vaccination with inactivated influenza A virus (IAV) and were responsible for protect
97   When hemagglutinin (HA) glycoproteins from influenza A virus (IAV) are expressed in cells, ER stres
98                                              Influenza A virus (IAV) can adapt to poultry and mammali
99                                              Influenza A virus (IAV) causes an acute infection in hum
100                                              Influenza A virus (IAV) causes annual epidemics and occa
101                                              Influenza A virus (IAV) causes up to half a million deat
102 y CD4 T cell recall following heterosubtypic influenza A virus (IAV) challenge of mice primed previou
103                                The genome of influenza A virus (IAV) comprises eight RNA segments (vR
104                                              Influenza A virus (IAV) consists of eight viral RNA (vRN
105                                              Influenza A virus (IAV) continues to pose an enormous an
106     One of the major unresolved questions in influenza A virus (IAV) ecology is exemplified by the ap
107                 The matrix protein 1 (M1) of influenza A virus (IAV) exists as a three-dimensional ol
108                                              Influenza A virus (IAV) expresses m(6)A-modified RNAs, b
109                                              Influenza A virus (IAV) genomes are composed of eight si
110                   The emergence of the novel influenza A virus (IAV) H7N9 since 2013 has caused conce
111 th threat of animal to human transmission of influenza A virus (IAV) has stimulated interest in rapid
112          We have shown that glycosylation of influenza A virus (IAV) hemagglutinin (HA), especially a
113                      Using a murine model of influenza A virus (IAV) infection and a panel of chromos
114 allergic inflammation was protective against influenza A virus (IAV) infection and disease.
115    Exaggerated inflammatory responses during influenza A virus (IAV) infection are typically associat
116 ility of human alveolar macrophages (AMs) to influenza A virus (IAV) infection in comparison with aut
117 he outcome of infectious diseases, including influenza A virus (IAV) infection, are rarely evaluated.
118  respiratory epithelial cells in response to influenza A virus (IAV) infection, as well as the CHIP-s
119 es in our understanding of the mechanisms of influenza A virus (IAV) infection, the crucial virus-hos
120 empers the intensity of the host response to influenza A virus (IAV) infection.
121 nspecific protection has been observed after influenza A virus (IAV) infection.
122                                              Influenza A virus (IAV) infections cause major morbidity
123    We then apply our method to a data set of influenza A virus (IAV) infections for which viral deep-
124                          The pathogenesis of influenza A virus (IAV) infections is a multifactorial p
125 fections increase morbidity and mortality of influenza A virus (IAV) infections.
126                                              Influenza A virus (IAV) is a lytic virus in primary cult
127                                              Influenza A virus (IAV) is an RNA virus that is cytotoxi
128 s of infections, but its role in immunity to influenza A virus (IAV) is not well studied.
129                          A unique feature of influenza A virus (IAV) life cycle is replication of the
130 ing it with the well-characterized viroporin influenza A virus (IAV) matrix-2 protein.
131                                              Influenza A virus (IAV) nonstructural protein 1 (NS1) is
132                                              Influenza A virus (IAV) of the H3 subtype is an importan
133  human A549 cells from lethal infection with influenza A virus (IAV) or vesicular stomatitis virus (V
134    Asia is considered an important source of influenza A virus (IAV) pandemics, owing to large, diver
135 S and human and mouse genetics, we show that influenza A virus (IAV) ribogenesis and growth are suppr
136                                              Influenza A virus (IAV) RNA packaging signals serve to d
137 e T cells in children to genetically diverse influenza A virus (IAV) strains to which the children ha
138 he mechanisms that are being utilized by the Influenza A virus (IAV) to induce host shutoff.
139 rcoma-associated herpesvirus (KSHV), against influenza A virus (IAV) were investigated in vitro and i
140              PB1-F2 is a virulence factor of influenza A virus (IAV) whose functions remain misunders
141                      Here, we show that that influenza A virus (IAV) with maximised frequencies of th
142                              Two subtypes of influenza A virus (IAV), avian-origin canine influenza v
143 SV-1), encephalomyocarditis virus (EMCV) and influenza A virus (IAV), we identified several TRIM prot
144 e, we track the number and phenotype of four influenza A virus (IAV)-specific CTLp populations in nai
145 d virus Epstein-Barr virus (EBV), as well as influenza A virus (IAV).
146 g infection, including RNA and proteins from influenza A virus (IAV).
147 broad protection against distinct strains of influenza A virus (IAV).
148 or detrimental at different stages of lethal influenza A virus (IAV).
149 he emergence of drug resistance mutations in influenza A virus (IAV).
150  control of enveloped RNA viruses, including influenza A virus (IAV).
151 ding protein 1 (ZBP1) as an innate sensor of influenza A virus (IAV).
152 ed mortality after infectious challenge with influenza A virus (IAV).
153 to humans have enhanced the virulence of the influenza A virus (IAV).
154                                        Swine influenza A viruses (IAV) are a major cause of respirato
155                                              Influenza A viruses (IAV) are zoonotic pathogens that po
156                                              Influenza A viruses (IAV) can cause lung injury and acut
157 between H5 or H9 subtype avian and mammalian influenza A viruses (IAV) can generate a novel virus tha
158 ng to the genetic and antigenic diversity of influenza A viruses (IAV) currently circulating in swine
159                                              Influenza A Viruses (IAV) in nature must overcome shifti
160 ckaging of the eight genomic RNA segments of influenza A viruses (IAV) into viral particles is coordi
161                                 Two zoonotic influenza A viruses (IAV) of global concern, H5N1 and H7
162                                        Avian influenza A viruses (IAV) of the H9N2 subtype have succe
163 ope tag in the C terminus of PB1 resulted in influenza A viruses (IAV) that are safe and effective as
164  interactomes between human host and several influenza A viruses (IAV).
165 ne are one of the main reservoir species for influenza A viruses (IAVs) and play a key role in the tr
166 uenza virus pathogenesis.IMPORTANCE Seasonal influenza A viruses (IAVs) are among the most common cau
167 ion of genetically and antigenically diverse influenza A viruses (IAVs) are circulating among the swi
168                                              Influenza A viruses (IAVs) are endemic in swine and repr
169 ve vaccine approaches against IAV.IMPORTANCE Influenza A viruses (IAVs) are one of the most common ca
170  key role in the ecology and transmission of influenza A viruses (IAVs) between species.
171 reassortment is segment dependent.IMPORTANCE Influenza A viruses (IAVs) can exchange genes through re
172 sonal influenza viruses in humans.IMPORTANCE Influenza A viruses (IAVs) cause acute infection of the
173                                              Influenza A viruses (IAVs) cause seasonal epidemics and
174                                              Influenza A viruses (IAVs) continue to threaten animal a
175 n variability in subjects infected with H3N2 influenza A viruses (IAVs) during the 2010/2011 season w
176 ortment of gene segments between coinfecting influenza A viruses (IAVs) facilitates viral diversifica
177 equenced the genomes of 441 wild-bird origin influenza A viruses (IAVs) from North America and subjec
178  are critical for activating HAs of seasonal influenza A viruses (IAVs) in humans.
179 ) that neutralizes both group I and group II influenza A viruses (IAVs) in vitro.
180                                    Different influenza A viruses (IAVs) infect the same cell in a hos
181                The risk of emerging pandemic influenza A viruses (IAVs) that approach the devastating
182 sights into the mechanisms of replication of influenza A virus in ducks.
183                  The emergence of avian H7N9 influenza A virus in humans with associated high mortali
184 anding the underlying population dynamics of influenza A viruses in commercial and exhibition swine i
185 the disease-causing potential of LP avian H7 influenza A viruses in mammals may be underestimated, an
186            Since the emergence of human H3N2 influenza A viruses in the pandemic of 1968, these virus
187 tiviral efficacy against multidrug-resistant influenza A viruses, in vitro drug resistance barrier, a
188 y against several human clinical isolates of influenza A viruses, including both oseltamivir-sensitiv
189 ne are actively involved in the evolution of influenza A viruses, including zoonotic strains.
190 to pigs resulted in substantial evolution of influenza A viruses infecting swine, contributing to the
191 ding EPS15 at endosomes, thereby influencing influenza A virus infection as well as degradation of EG
192 ceptives, levonorgestrel, impacts sequential influenza A virus infection by modulating antibody respo
193 e to the increased morbidity associated with influenza A virus infection during pregnancy.
194 s and plasmacytoid dendritic cells (pDCs) to influenza A virus infection in 21 pregnant and 21 nonpre
195         Although it is well established that Influenza A virus infection is initiated in the respirat
196 mune-competent children and that a preceding influenza A virus infection may not provide cross-protec
197                Susceptibility to colitis and influenza A virus infection occurring upon commensal bac
198 describe the imprinting by the initial first influenza A virus infection on the antibody response to
199 ed influenza, we identified 13 children with influenza A virus infection who were subsequently infect
200 sponses are important for protection against influenza A virus infection, that these can be most effi
201 uate the microminipig as an animal model for influenza A virus infection, we compared the receptor di
202 ficantly affect adaptive immune responses to influenza A virus infection, with their effect on the ou
203 the microminipig as a novel animal model for influenza A virus infection.
204 ipig could serve as a novel model animal for influenza A virus infection.
205 ntribute to pulmonary inflammation following influenza A virus infection.
206 mponents and TLR3 as crucial for immunity to influenza A virus infection.
207 S2 plays an important and unexpected role in influenza A virus infection.
208 ecognition by the immune system during human influenza A virus infection.
209 es the ThCTL that develop in the lung during influenza A virus infection.
210 ominipigs represent a novel animal model for influenza A virus infection.
211 ed to an elevated cellular susceptibility to influenza A virus infection.
212 etween younger and aging mice in response to influenza A virus infection.IMPORTANCE Influenza virus i
213  Furthermore, we demonstrate that herpes and influenza A virus infections are enhanced when host circ
214          Emerging evidence from vaccinia and influenza A virus infections indicates that subsets of c
215 ugs used for the prevention and treatment of influenza A virus infections.
216 fluenza B virus infections than for treating influenza A virus infections.
217                            Together with the influenza A virus, influenza B virus causes seasonal flu
218  positive and negative percent agreement for influenza A virus, influenza B virus, and RSV were 79.2%
219  influenza epidemics that can be severe, and influenza A viruses intermittently cause pandemics.
220 e identified 10 independent introductions of influenza A virus into Ohio and/or Indiana exhibition sw
221                                              Influenza A virus is a human pathogen whose genome is co
222                                              Influenza A virus is a human pathogen with a genome comp
223 y to promote their nuclear export.IMPORTANCE Influenza A virus is a major pathogen of a wide variety
224                                              Influenza A virus is a threat for humans due to seasonal
225 ergetic barrier to pore expansion.IMPORTANCE Influenza A virus is an airborne pathogen causing season
226                     The M2 proton channel of influenza A virus is an integral membrane protein involv
227                                              Influenza A virus is characterized by high genetic diver
228 ain-specific neutralizing antibodies against influenza A virus is known to confer potent protection a
229 sm underlying the genetic diversification of influenza A virus is reassortment of intact gene segment
230                              Reassortment of influenza A viruses is an important driver of virus evol
231                              Reassortment of influenza A viruses is readily observed during coinfecti
232                            The RNA genome of influenza A viruses is transcribed and replicated by the
233 ain, implicated in host range restriction of influenza A viruses, is still poorly understood.
234                    Similarly, challenge with influenza A virus led to increased infiltration of the v
235  role for cellular chaperone Hsp40/DnaJB1 in influenza A virus life cycle by assisting nuclear traffi
236                                          The influenza A virus M1 and M2 proteins play important role
237 ell epitope from the extracellular domain of influenza A virus M2 protein (M2e).
238  identified a mutation at position 76 of the influenza A virus M2 protein that drastically reduces in
239  results suggest that PB1-F2 from H7N9 avian influenza A virus may be a major contributory factor to
240                                              Influenza A virus mRNAs are transcribed by the viral RNA
241 e pandemic threat posed by emerging zoonotic influenza A viruses necessitates development of antivira
242                             In contrast, the influenza A virus NS1 protein interacts with RIG-I and T
243                                          The influenza A virus nucleoprotein (NP) is an essential mul
244 we identify several acetylation sites of the influenza A virus nucleoprotein (NP), including the lysi
245  host species, cross-species transmission of influenza A viruses occurs occasionally.
246 ns in 2012 and the widespread circulation of influenza A viruses of the same genotype in exhibition s
247                            Attachment of the Influenza A virus onto host cells involves multivalent i
248                             The threat of an influenza A virus pandemic stems from continual virus sp
249 reactive oxygen species production abrogates influenza A virus pathogenicity.
250                                        Avian influenza A virus polymerases typically do not function
251 then coinfected them with mouse-adapted H1N1 influenza A virus (PR/8/34).
252                VX-787 is an inhibitor of the influenza A virus pre-mRNA cap-binding protein PB2.
253 sible reassortment of human and other animal influenza A viruses presents an ongoing risk to public h
254    Specifically, we inoculated 2D2 mice with influenza A virus (Puerto Rico/8/34; PR8) and then monit
255                        To understand how the Influenza A virus RdRp coordinates these processes, we a
256                        To understand how the influenza A virus RdRp coordinates these processes, we a
257                                          The Influenza A virus RdRp in contrast, uses a capped RNA ol
258                                          The influenza A virus RdRp, in contrast, uses a capped RNA o
259 nsider the constraints and drivers acting on influenza A virus reassortment, including the likelihood
260  PB1, PB2, and PA is necessary for efficient influenza A virus replication in new host species.
261           Exogenous SPL expression inhibited influenza A virus replication, which correlated with an
262  role for TRIM25 in specifically restricting influenza A virus replication.
263                   An interaction between the influenza A virus RNA polymerase and the C-terminal doma
264 all, this work advances our understanding of influenza A virus RNA synthesis and identifies the initi
265 all, this work advances our understanding of Influenza A virus RNA synthesis and identifies the initi
266 G repeats, which has some resemblance to the influenza A virus shift site, triggers the +1 frameshift
267 ng CD4 effector population, and they mediate influenza A virus-specific cytotoxic activity.
268                         Here, we examine the influenza A virus spike protein hemagglutinin (HA), whic
269                                     Like all influenza A virus strains, A(H5N1) viruses evolve rapidl
270  the N-truncated NS1 proteins encoded by two influenza A virus strains, Udorn/72/H3N2 (Ud) and Puerto
271 alization of PB2 of human from that of avian influenza A virus strains.
272 virus, in 1958, 16 different novel, zoonotic influenza A virus subtype groups in 29 countries, Taiwan
273 le anilines were identified as inhibitors of influenza A virus subtype H1N1, and extensive chemical s
274                                          Two influenza A virus subtypes has been reported in dogs in
275 r cases of human infection by emerging avian influenza A virus subtypes, including H7N9 and H10N8 vir
276                                              Influenza A virus suppresses the translation of host mRN
277                               Through active influenza A virus surveillance in US exhibition swine an
278 ists in more than 95% of current circulating influenza A viruses, targeting the AM2-S31N proton chann
279 .39a effectively neutralized the majority of influenza A viruses tested, representing 16 HA subtypes.
280 -S31N inhibitors were active against several influenza A viruses that are resistant to one or both cl
281                                          New influenza A viruses that emerge frequently elicit compos
282     Avian H7N9 influenza viruses are group 2 influenza A viruses that have been identified as the eti
283 ) is a sialidase expressed on the surface of influenza A viruses that releases progeny viruses from t
284                                              Influenza A viruses that successfully established stable
285 ssion of influenza A(H7N2), an avian-lineage influenza A virus, that occurred during an outbreak amon
286  vessel for the generation of novel pandemic influenza A viruses through reassortment because of thei
287  proteins encoded by the current circulating influenza A viruses; thus, it represents a high-profile
288 NA plays an important role in the ability of influenza A virus to replicate in duck intestine.
289 ary for introduction and adaptation of avian influenza A viruses to mammalian hosts is important for
290              The role of exhibition swine in influenza A virus transmission was recently demonstrated
291     In this paper, the prospect of detecting influenza A virus using digital ELISA has been studied.
292            The only licensed live attenuated influenza A virus vaccines (LAIVs) in the United States
293 nsitivity of the Alere test for detection of influenza A virus was likely due to a study set that inc
294 und that the sensitivity of microminipigs to influenza A viruses was the same as that of larger minia
295 pig, and the sensitivity of microminipigs to influenza A viruses was the same as that of miniature pi
296                             Coinfection with influenza A virus, which also expresses a neuraminidase,
297  whole genome sequencing (HT-WGS) method for influenza A viruses, which utilized an enzymatic cleavag
298 ong distances indicate that novel strains of influenza A virus will continue to emerge and spread wit
299                                         Most influenza A viruses with known subtype were A(H3N2) (570
300 can wild birds are an important reservoir of influenza A viruses, yet the potential of viruses in thi

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