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1 genically distinct, influenza glycoproteins (hemagglutinins).
2 conserved stalk domain of influenza B virus hemagglutinin.
3 shared with the 2009 pandemic H1N1 (Cal/04) hemagglutinin.
4 utralizing antibodies target influenza virus hemagglutinin.
5 taneously inducing high levels of Abs toward hemagglutinin.
6 anes of fibroblast cells that stably express hemagglutinin.
7 onserved stalk domain of the influenza virus hemagglutinin.
8 tralizing humoral immunity against the viral hemagglutinin.
9 tralizing humoral immunity against the viral hemagglutinin.
10 n of potent peptidic inhibitors of influenza hemagglutinin.
11 H5N8 (H5Nx) viruses containing the Eurasian hemagglutinin 2.3.4.4 clade from wild bird populations i
12 ric assessment of binding thermodynamics for hemagglutinin 306-319 peptide variants to the human MHC
13 shown to describe fusion by influenza virus hemagglutinin (a "class I" fusogen) and West Nile virus
15 s found to utilize a relatively lower pH for hemagglutinin activation, similar to human influenza vir
16 ttering experimental data of the filamentous hemagglutinin adhesin beta-barrel protein transporter so
17 reater Fc receptor activity to pandemic H1N1 hemagglutinin after the swine influenza pandemic of 2009
19 image the distributions of antibody-labeled hemagglutinin and isotope-labeled cholesterol and sphing
20 controlled by cohesive interactions between hemagglutinin and liquid-ordered domains enriched with c
23 assortments of H5 and H6N6 viruses, with the hemagglutinin and neuraminidase combinations being stron
24 ained with recombinant proteins for both the hemagglutinin and neuraminidase indicate a true avian re
25 luated if a reassortant virus containing the hemagglutinin and neuraminidase of A/quail/Hong Kong/G1/
26 rly, antibody titers against influenza virus hemagglutinin and neuraminidase significantly decreased
27 ntibodies to the viral surface glycoproteins hemagglutinin and neuraminidase, and these responses can
28 a and IL-17-producing cells specific for the hemagglutinin and nucleocapsid proteins appeared in circ
29 nonsynonymous genetic diversity in the viral hemagglutinin and nucleoprotein, and (iii) intrahost vir
30 phtheria toxin, pertussis toxin, filamentous hemagglutinin and pertactin were measured at 14 and 24 w
31 ort physiologically relevant binding of H3N2 hemagglutinin and that this physiologically relevant bin
32 ly targeted the conserved stalk region of H1 hemagglutinin and was effective against drug-resistant H
33 titutes a novel method of escape for group 1 hemagglutinins and could represent an alternative means
34 to pertussis toxin, antibody to filamentous hemagglutinin, and antibody to pertactin were measured i
37 and alpha-GalCer induced high titers of anti-hemagglutinin antibodies and generated virus-specific T
38 was defined as >/=4-fold increase in paired hemagglutinin antibody inhibition titers from 1 month po
39 ertussis toxin (anti-PT) or anti-filamentous hemagglutinin antibody titers, and by genetic testing (p
40 nt adjuvants for recombinant influenza virus hemagglutinin antigen induction of humoral and cellular
41 unization with this adjuvant and recombinant hemagglutinin antigen is transferable with serum from im
43 red influenza vaccines that express chimeric hemagglutinin antigens offer a novel means for protectin
45 We tested this hypothesis using influenza hemagglutinin as a model viral antigen and transgenic, M
49 l antibody against conserved epitopes of the hemagglutinin can be combined with TIV to elicit broad p
51 l of influenza A viruses expressing chimeric hemagglutinins (cHA) with intragroup or intergroup head/
52 r from specific binding interactions between hemagglutinin, cholesterol, and/or the majority of sphin
55 strains showing a different insertion at the hemagglutinin cleavage site, as well as nine nucleotide
58 otective vaccine candidate based on chimeric hemagglutinins, consisting of globular head domains from
59 NK cells by human IgG-opsonized influenza A hemagglutinin correlated with dimeric rsFcgammaRIIIa bin
61 ime-boost influenza vaccine trial, we sorted hemagglutinin cross-reactive memory B cells and identifi
64 nerally agreed with the surface glycoprotein hemagglutinin esterase phylogeny, were observed between
67 e, we present the crystal structures of ISAV hemagglutinin-esterase unbound and complexed with recept
71 e fusion assay, using transfected fusion and hemagglutinin expression plasmids or with syncytium-base
72 mbinant pertussis toxin (PT) and filamentous hemagglutinin (FHA) were assessed by enzyme-linked immun
73 es against pertussis toxin (PT), filamentous hemagglutinin (FHA), pertactin (Prn), tetanus toxoid (TT
76 than twofold increase in the affinity of its hemagglutinin for mammalian receptors: the model predict
77 nfection or vaccination with VLPs containing hemagglutinin from A/PR8/34 influenza virus induced high
78 s and glycan microarray data for recombinant hemagglutinins from A(H6N1) and A(H10N8) viruses, isolat
79 , and that immunization with influenza virus hemagglutinin fused to hXCL1 or hXCL2 induced full prote
81 in can be substituted by the influenza virus hemagglutinin fusion peptide, and this chimera also acti
82 that membrane remodeling commenced with the hemagglutinin fusion protein spikes grappling onto the t
86 an H7N9 formulation containing 15 microg of hemagglutinin given without adjuvant, with AS03 adjuvant
88 en accompanied by glycan accumulation on the hemagglutinin globular head, and hemagglutinin receptor
90 MR, 0.89; 95% CI, 0.87-0.90) and filamentous hemagglutinin (GMR, 0.89; 95% CI, 0.88-0.90) and 22% low
91 target cells by coordinated action of the MV hemagglutinin (H) and fusion (F) envelope glycoproteins;
93 to determine the glycosylation of Influenza hemagglutinin (H1/A/California/04/2009) using the follow
96 bulin (Ig) 2D1 is effective against the 1918 hemagglutinin (HA) and also known to cross-neutralize th
97 epitope in the vestigial esterase domain of hemagglutinin (HA) and blocks HA-mediated membrane fusio
99 urally defined interaction between influenza hemagglutinin (HA) and its cell surface receptor sialic
100 by reverse genetics using the wild-type (wt) hemagglutinin (HA) and neuraminidase (NA) genes from the
102 ions of the influenza virus surface proteins hemagglutinin (HA) and neuraminidase (NA) is thought to
104 the interaction of the surface glycoproteins hemagglutinin (HA) and neuraminidase (NA) with the cell
107 monoclonal antibody, m826, that binds to H7 hemagglutinin (HA) and protects against H7N9 infection.
108 ltivalent interactions between virus surface hemagglutinin (HA) and sialoside-containing glyco ligand
110 f-amplifying mRNA expressing influenza virus hemagglutinin (HA) antigen [SAM(HA)] formulated with a n
111 f computationally optimized broadly reactive hemagglutinin (HA) antigens (COBRA) for H1N1 isolates.
113 dity trimeric proteins that bind influenza A hemagglutinin (HA) at its conserved receptor binding sit
117 kers and their predicted phenotypic effects, hemagglutinin (HA) clade classifications, an automated t
118 plasmic tail of influenza virus glycoprotein hemagglutinin (HA) contains three cysteines, posttransla
122 irus vaccines rely on the antigenic match of hemagglutinin (HA) for vaccine strain selection, and mos
123 ibodies against tetanus toxoid and influenza hemagglutinin (HA) from H1N1 and newly emergent subtypes
125 f adenovirus serotype 6 (Ad6) to express the hemagglutinin (HA) gene from influenza A/PR/8/34 virus.
126 as used to determine genetic group, based on hemagglutinin (HA) gene sequences, of influenza A(H3N2)
128 iruses continuously acquire mutations in the hemagglutinin (HA) glycoprotein that abrogate binding of
129 primarily focused on the head region of the hemagglutinin (HA) glycoprotein, which in turn undergoes
130 mune responses to influenza virus target the hemagglutinin (HA) glycoprotein, which is the major anti
131 o cell surface sialic acid receptors via the hemagglutinin (HA) glycoprotein, with the neuraminidase
133 The majority of these antibodies bind to the hemagglutinin (HA) head domain and function by blocking
137 antibodies against the surface glycoprotein hemagglutinin (HA) is the primary method used to control
140 antibodies to the 'stem' of influenza virus hemagglutinin (HA) now allow us to incorporate into simu
143 L chain usage of the Ab response against the hemagglutinin (HA) protein elicited by influenza infecti
146 t a single amino acid at position 158 of the hemagglutinin (HA) protein substantially affected the sy
147 umulation of amino acid substitutions in the hemagglutinin (HA) protein, resulting in escape from pri
148 y, where virions with relatively acid-stable hemagglutinin (HA) proteins are rendered incapable of pH
149 First, we tested the binding of recombinant hemagglutinin (HA) proteins of seal H3N8 and human-adapt
150 a between 2005 and 2015, particularly at the hemagglutinin (HA) proteolytic cleavage site (PCS) that
151 lates, have a leucine at position 226 in the hemagglutinin (HA) receptor binding site, which is criti
152 rimentally introduced mutations in the viral hemagglutinin (HA) receptor-binding domain conferred bin
155 ected against the stalk domains of the viral hemagglutinin (HA) show promise for protecting against d
156 man monoclonal antibody (hMAb) targeting the hemagglutinin (HA) stalk offers a promising approach to
157 reactive antibodies targeting the conserved hemagglutinin (HA) stalk region are elicited following s
160 eutralizing antibodies (bnAbs) targeting the hemagglutinin (HA) stem revitalized hopes of developing
161 ing human antibodies targeting the influenza hemagglutinin (HA) stem, with exceptional neutralizing b
163 protection against severe disease from novel hemagglutinin (HA) subtypes in the same phylogenetic gro
164 embers of a subgroup (H7-H10-H15) of group 2 hemagglutinin (HA) subtypes that include H7N9 and H10N8
167 pandemics require that a virus containing a hemagglutinin (HA) surface antigen previously unseen by
168 ting specific antibody responses against the hemagglutinin (HA) surface glycoprotein; however, the di
170 antigenic site B of the surface glycoprotein hemagglutinin (HA) that explain the antigenic difference
173 ic analysis identified T-cell epitopes in H7 hemagglutinin (HA) which potentially enhance regulatory
175 rgely determined by the surface glycoprotein hemagglutinin (HA), and amino acid substitutions at expo
177 ion T401A occurred prior to substitutions in hemagglutinin (HA), causing the altered receptor-binding
178 hat glycosylation of influenza A virus (IAV) hemagglutinin (HA), especially at position N-27, is cruc
181 viruses of mice that had been immunized with hemagglutinin (HA), neuraminidase (NA) and the extracell
182 st H7N9 virus-infected cells and recombinant hemagglutinin (HA), neuraminidase (NA), and nucleoprotei
183 r example, in the influenza envelope protein hemagglutinin (HA), the low pH in the endosome triggers
184 terations in the viral surface glycoprotein, hemagglutinin (HA), typically are required for influenza
185 ing reverse genetics and fixing the CIV-H3N2 hemagglutinin (HA), we found that 51 of the 127 possible
186 fic mAbs target the head domain of the viral hemagglutinin (HA), whereas broadly reactive mAbs typica
187 examine the influenza A virus spike protein hemagglutinin (HA), which undergoes a dynamic conformati
188 sights into the mechanisms by which chimeric hemagglutinin (HA)-based vaccines confer immunity, namel
191 measured by a microneutralization assay, and hemagglutinin (HA)-specific and nucleoprotein (NP)-speci
192 Longitudinal tracking of vaccination-induced hemagglutinin (HA)-specific clones revealed no overall i
198 IBV are distinguished, based on variation in hemagglutinin (HA): B/Victoria/2/87-like (B/Vic) and B/Y
199 determining the structure of influenza-virus hemagglutinin (HA):single-chain variable-domain fragment
201 icenter trial of RIV4 (45 mug of recombinant hemagglutinin [HA] per strain, 180 mug of protein per do
202 mplifies the most critical genomic segments (hemagglutinin [HA], neuraminidase [NA], and matrix [M])
203 1N1]pdm09) and avian influenza A(H7N9) virus hemagglutinins (HAs) despite being seronegative for thes
204 -reactive antibodies showed broad binding to hemagglutinins (HAs) from previously circulating virus s
206 ntaining wild-type and mutant MN/10 or BJ/92 hemagglutinins (HAs) were constructed and probed for rea
207 Receptor-binding preference and stability of hemagglutinin have been implicated as crucial determinan
208 : fusion protein (F) and attachment proteins hemagglutinin, hemagglutinin-neuraminidase, or glycoprot
211 responses to tetanus toxin but not influenza hemagglutinin in the ART group were lower than those in
212 s anthracis protective antigen and influenza hemagglutinin-in which B cells competed both intra- and
213 across nine different amino acid residues in hemagglutinin including seven that have not been describ
214 ent adjuvant for recombinant influenza virus hemagglutinin, inducing rapid and sustained immunity tha
215 ibition of adhesion: the model predicts that hemagglutinin inhibitors of relatively modest affinity c
216 We therefore speculate that local sterol-hemagglutinin interactions in the viral envelope may con
219 le amino acid residue substitution in NY1682 hemagglutinin is responsible for the difference in infec
222 ecipient mice after the cocapture of MOG and hemagglutinin leads to the production of class-switched
223 When applied to the adhesion between the hemagglutinin ligands on influenza viruses and the siali
224 esicular stomatitis virus (VSV) encoding the hemagglutinin-like envelope glycoproteins HL17 or HL18 i
227 e 11th gene of the 16-gene mannose-sensitive hemagglutinin (MSHA) type IV pilus operon), had reduced
228 glycoproteins: an attachment protein called hemagglutinin-neuraminidase (HN [also called H or G depe
229 the sequences of the Small Hydrophobic (SH), Hemagglutinin-Neuraminidase (HN) and Fusion (F) genes of
230 ajor attachment glycoprotein (G) between the hemagglutinin-neuraminidase (HN) and RNA-dependent RNA p
231 eign gene at the PIV5 small hydrophobic (SH)-hemagglutinin-neuraminidase (HN) junction or deletion of
233 ated action of the receptor-binding protein, hemagglutinin-neuraminidase (HN), and the fusion protein
234 cleavage site, F117S (F117S), and another in hemagglutinin-neuraminidase (HN), G169R (HN169R), locate
235 orchestrated by the receptor binding protein hemagglutinin-neuraminidase (HN; also called H or G depe
236 teins: the attachment glycoprotein (G, H, or hemagglutinin-neuraminidase [HN]) and the fusion glycopr
237 n (F) and attachment proteins hemagglutinin, hemagglutinin-neuraminidase, or glycoprotein (G), which
238 onstructed mutants with substitutions in the hemagglutinin of A/Netherlands/602/09 in an attenuated b
239 amino acid substitutions was observed in the hemagglutinin of H7 AIVs from waterfowl and domestic pou
241 mmunization with an immunologically distinct hemagglutinin of the same subtype offers the potential t
243 g to quadrivalent formulations including the hemagglutinins of influenza A subtypes H1N1 and H3N2 and
244 inin trimers, so the spatial distribution of hemagglutinin on the viral envelope may influence fusion
245 y later than particles bearing the influenza hemagglutinin or GP from lymphocytic choriomeningitis vi
246 o the RepRNA (luciferase, or influenza virus hemagglutinin or nucleoprotein) could decrease, while th
247 (hemagglutinin receptor binding specificity, hemagglutinin pH of activation, and polymerase complex e
248 s mutations to reproduce influenza's spindly hemagglutinin phylogeny, co-circulation of antigenic var
250 C-Ads generate markedly more influenza virus hemagglutinin protein and require substantially less vec
251 the conserved receptor-binding pocket of the hemagglutinin protein and to match the trimeric nature o
257 paper-based influenza assay that targets the hemagglutinin protein; the assay employs a combination o
258 omplexity and leveraging the large number of hemagglutinin proteins on the surface of each virus.
259 tion on the hemagglutinin globular head, and hemagglutinin receptor binding has changed from recognit
261 three specific traits of influenza viruses (hemagglutinin receptor binding specificity, hemagglutini
262 actors essential for processing of the virus hemagglutinin represent very suitable drug targets becau
264 tructure and receptor specificity of the H15 hemagglutinin, revealing distinct features and specifici
265 crease in ADCC-Ab titers to both recombinant hemagglutinin (rHA) protein and homologous virus-infecte
266 VA peptide, and the alpha-helix of influenza hemagglutinin's stem; the last afforded protection again
269 tative estimate of the affinity range of the hemagglutinin-sialic acid interaction necessary for the
270 t pandemic H1N1 influenza virus in which the hemagglutinin signal sequence has been suppressed (S-FLU
271 urther find that sterol-dependent changes to hemagglutinin spatial patterning in the viral membrane d
272 arrow-derived radioresistant cells to induce hemagglutinin-specific antibodies and protect mice again
273 lacked robust clonal expansion of influenza hemagglutinin-specific B cells early after infection and
274 sequence, MOG-specific B cells get help from hemagglutinin-specific T cells to produce anti-MOG antib
276 d virus-neutralizing antibody titers but not hemagglutinin stalk antibody titers were lower in proges
277 uenza virucide that specifically targets the hemagglutinin stalk region, similar to targeting of anti
278 arget membrane dimpling as local clusters of hemagglutinin started to undergo conformational refoldin
280 antibodies (HV1-69-sBnAb) to the influenza A hemagglutinin stem domain has been clearly established.
284 tigenic cartography of all H3N2 viruses with hemagglutinin (the glycoprotein on the surface of the in
285 ds (S3-G4) showed the strongest binding to a hemagglutinin trimer (dissociation constant of 1.6 x 10(
286 s at near-atomic resolution of the influenza hemagglutinin trimer, which adopts a highly preferred sp
289 Optimal fusion likely requires multiple hemagglutinin trimers, so the spatial distribution of he
290 for a homologue of the temperature-sensitive hemagglutinin (Tsh) autotransporter described in avian E
292 e antigens cytomegalovirus pp65 or influenza hemagglutinin were able to present the antigens to autol
294 lls and memory B cells specific to influenza hemagglutinin were primarily observed in the mediastinal
295 clustering or spatial rearrangement of viral hemagglutinin, which affects the rate-limiting step of p
296 n, and no changes were observed in the viral hemagglutinin, which is the receptor attachment protein.
297 Understanding site specific glycosylation of hemagglutinin will increase our knowledge about virus ev
298 3-adjuvanted vaccines (low or medium dose of hemagglutinin with AS03A or AS03B), one nonadjuvanted va
299 rog, 7.5 microg, 15 microg, and 45 microg of hemagglutinin with or without AS03 or MF59 adjuvant mixe
300 clusters of the influenza envelope protein, hemagglutinin, within the plasma membrane are hypothesiz
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