ライフサイエンスコーパス: viral antigen

1 Rs) on immune cells upon binding of tumor or viral antigen.

2 AT1 in bystander cells staining negative for viral antigen.

3 esentation of the intracellular reservoir of viral antigen.

4 ction have reported systemically distributed viral antigen.

5 liferation that correlated with abundance of viral antigen.

6 al for both sampling and presenting residual viral antigen.

7 ells to produce interleukin 2 in response to viral antigen.

8 e new neutralizing antibodies to the mutated viral antigen.

9 a homologous and potentially cross-reactive viral antigen.

10 timulates a state of unresponsiveness toward viral antigens.

11 LN (DLN) by dendritic cells (DCs) presenting viral antigens.

12 Rs) that were able to recognize both MBP and viral antigens.

13 machinery for MHC II presentation of herpes viral antigens.

14 ies and by tissue colocalization of distinct viral antigens.

15 l CD8(+) T-cell responses to HIV-1 and other viral antigens.

16 yielded >300 unique antibodies against H5N1 viral antigens.

17 ne effectors that mediate rapid responses to viral antigens.

18 es on the immune responses to endogenous and viral antigens.

19 n a second lipid membrane containing several viral antigens.

20 fic T cells specific for tumor-associated or viral antigens.

21 since they lack expression of immunodominant viral antigens.

22 dy to both measles (P=.08) and mumps (P=.03) viral antigens.

23 h promoters are active in the absence of any viral antigens.

24 N-gamma and availability of newly translated viral antigens.

25 the cross-reactivity of seven mosquito-borne viral antigens.

26 in re-challenge experiments), and respond to viral antigens.

27 nerated especially strong responses to lytic viral antigens.

28 infected iPSCs induced de novo expression of viral antigens.

29 -gamma) and availability of newly translated viral antigens.

30 duration, implying prolonged presentation of viral antigens.

31 ncer germline antigen, rather than canonical viral antigens.

32 of viral infections and tumors that express viral antigens.

33 lture before search for the viral genome and viral antigens.

34 ses by mediating destruction of host IgG and viral antigens.

35 for oral HPV infection or seroreactivity to viral antigens.

36 uences, selected cancer testis antigens, and viral antigens.

37 acterial and fungal antigens, but not common viral antigens; (2) Th17 cells are infected by HIV in vi

38 lles, where it strongly colocalized with the viral antigen 2B and mature virions but not double-stran

39 HIKV infection confirmed by RT-qPCR (52.9%), viral antigen (41.1%), and/or specific-IgM (63.2%).

40 parental MP-12 induced neither IFN-alpha nor viral-antigen accumulation at the draining lymph node ye

41 In viral antigen (Ag)-positive cells, although the developm

42 A viral antigen against which the IgG in MS brain and CSF

43 r both strains, expressing the full range of viral antigens (Ags) and producing relatively large numb

44 s LRTI demonstrated an extensive presence of viral antigen and a near absence of CD8-positive lymphoc

45 ve lower airway inflammation with persistent viral antigen and cellular infiltrates.

46 led to endothelial destruction only required viral antigen and did not require infectious virus.

47 ly suppress MHV68 replication, thus limiting viral antigen and facilitating an effective gammaherpesv

48 Despite the high levels of viral antigen and inflammatory cell infiltration in the

49 Once there, LNDCs acquired viral antigen and initiated activation of viral specific

50 esident meningeal macrophages (MMs) acquired viral antigen and interacted directly with infiltrating

51 Viral antigen and RNA staining decreased in targeted and

52 this mechanism to cross-present circulating viral antigen and showed that moDCs from chronically inf

53 Irf5(-/-) mice were associated with abundant viral antigen and terminal deoxynucleotidyltransferase-m

54 sis using influenza hemagglutinin as a model viral antigen and transgenic, MOG-specific B cells.

55 Because Tax is the most immunogenic viral antigen and triggers strong CTL responses, our res

56 to the S phase.The interaction between early viral antigens and cell cycle regulators represents an i

57 ction as the cells became immunoreactive for viral antigens and cytopathic effect was observed.

58 ion of late but not immediate early or early viral antigens and had no appreciable effect on viral DN

59 py, HIV-1-infected cells continue to produce viral antigens and induce chronic immune exhaustion.

60 tiation of B cells that are not specific for viral antigens and instead encode antibodies that react

61 d colleagues reveal a mosaic distribution of viral antigens and nucleic acids and a mismatch between

62 overed a surprisingly mosaic distribution of viral antigens and nucleic acids.

63 ion in infected cells, when large numbers of viral antigens and potential immune modulators are expre

64 through their ability to capture and process viral antigens and subsequently induce adaptive immune r

65 ficiently and rapidly internalized exogenous viral antigens and then presented those antigens on majo

66 potential limitations of targeting a single viral antigen, and how to manage the patient with a viru

67 +) T cells driven to maturity by coinfecting viral antigens, and this physical proximity rather than

68 ening; identified new, frequently recognized viral antigens; and revealed a broader humoral response

69 These defects were due to viral antigen-antibody complexes and not the chronic inf

70 nce of LMP1-positive AR-DLBCL, cases without viral antigens appear able to avoid immunologic reaction

71 Importantly, both ACE-2 and viral antigen appeared to preferentially colocalize at t

72 -associated Burkitt's lymphomas, all but one viral antigen are repressed for immunoevasion.

73 odies, even though T-cell responses to major viral antigens are crucial when controlling viral replic

74 In fact, only a few viral antigens are detected in bronchial epithelial cell

75 the cornea and not in the stromal layer, and viral antigens are eliminated before stromal inflammatio

76 not clear what drives inflammation, whether viral antigens are necessary, or how viral antigens reac

77 This immune evasion strategy ensures that viral antigens are not presented on the cell surface dur

78 stic tests (RIDTs), immunoassays that detect viral antigens, are often used for diagnosis by physicia

79 fected lungs and that neutrophils expressing viral antigen as a result of direct infection by IAV exh

80 as associated with the increased presence of viral antigen as well as high levels of maturation marke

81 onse derived from the UCB graft is primed to viral antigens as early as day 42 after UCBT, but these

82 + T cell cytotoxicity against both tumor and viral antigens as well as intratumoral oHSV gene express

83 own by T cells bearing receptors that target viral antigens as well as T cells bearing re-engineered

84 ract infection of mice with influenza virus, viral antigen associated with dendritic cells (DCs) was

85 me and labor-intensive steps associated with viral antigen-based assays such as the observation of he

86 tes, thus reducing the capacity to eliminate viral antigen-bearing cells and slowing viral clearance.

87 eviously unrecognized interaction with MHC I-viral antigen-bearing pulmonary DCs in the lungs.

88 his approach by: (1) extending the number of viral antigens being targeted, (2) simplifying manufactu

89 cific CD8 T cells, while limiting amounts of viral antigen, both in hepatocyte-like cells and natural

90 ell-associated KSHV DNA, indicating that the viral antigen burden may have been driving these respons

91 ITH) by correlating regional neo-epitope and viral antigen burden with the regional adaptive immune r

92 multiple cytokines in response to persistent viral antigens but differed transcriptionally from memor

93 with reverse transcription PCR (RT-PCR) and viral antigen by immunofluorescence staining.

94 oughput siRNA screen based on detection of a viral antigen by microscopy to interrogate cellular prot

95 as a consequence of presentation of residual viral antigen by the migrant RDC.

96 vIL-10 alters the earliest host responses to viral antigens by dampening the magnitude and specificit

97 al protection after recognition of processed viral antigens by local DCs and B cells.

98 T cells isolated from the mice responded to viral antigens by producing gamma interferon when analyz

99 uggest that complement-mediated retention of viral antigens by stromal cells, such as follicular dend

100 Viral antigen can activate CD8 T cells, which in turn, c

101 us (SIV) vaccine vectors expressing the same viral antigens can elicit disparate T-cell responses.

102 reased in vitro cellular immune responses to viral antigens, CD4 and CD8 markers, and Th1-type cytoki

103 (T(N)) and central memory T cells (T(CM)) to viral antigen challenge in lymph nodes (LNs).

104 Vaccination with viral antigens combined with adjuvant correlated with th

105 ve EV71-specific ASC response to genogroup C viral antigens composed about 10% of the response.

106 bjects, including high-avidity antibodies to viral antigens, coverage against a panel of genetically

107 Moreover, this viral antigen-dependent maintenance results in a dramati

108 he previously infected lung capture residual viral antigen deposited in an irradiation-resistant cell

109 specific CD4(+) and CD8(+) T cells targeting viral antigens derived from Epstein-Barr virus (EBV) ind

110 to demonstrate the potential for multiplexed viral antigen detection and differentiation.

111 ntially, mass spectrometry-based methods for viral antigen detection may deliver higher throughput an

112 Rapid point-of-care viral antigen detection methods have been previously emp

113 and bead number on the assay sensitivity of viral antigen detection were studied.

114 tection, b) human antibody detection, and c) viral antigen detection, among which the viral gene dete

115 The large amount of circulating viral antigen did not impair or overactivate the S-CAR-g

116 lammatory mediators following recognition of viral antigen displaying cells.

117 Here, we demonstrate that viral antigen displaying neutrophils infiltrating the IA

118 A distinct viral antigen distribution in specific CNS cell types re

119 Viral antigen distribution in the respiratory tree, howe

120 rrelate the clinicopathological findings and viral antigen distribution with the genotypic characteri

121 tivation without altering the viral titer or viral antigen distribution.

122 sity (OD) of the test sample when reacted on viral antigen divided by the mean OD of the negative con

123 might corroborate the hypothesis of residual viral antigen-driven chronic arthritis.

124 s where they are capable of rapidly locating viral antigen, driving early activation of T cell popula

125 ation with the overlapping peptide pools for viral antigens EBNA1 and BZLF1, the number of responding

126 Cs specialized for T-cell activation acquire viral antigen either by becoming infected themselves (di

127 o no disease and no detectable expression of viral antigens even in non-parenchymal cells, indicating

128 resent soluble, cell-associated antigens and viral antigens even in the absence of Batf3.

129 ally assessed positional bias of epitopes in viral antigens, exploiting the large set of data availab

130 that in the broader immunological context of viral antigen exposure, the B cell response to variant i

131 ng expression of the more immunogenic latent viral antigens expressed in EBV type II and III latency

132 We also found significant heterogeneity of viral antigen expression across a large cohort, with man

133 ical analysis demonstrated similar levels of viral antigen expression but reduced activation of caspa

134 t is not known whether this heterogeneity of viral antigen expression could result in an uneven hepat

135 In many EBV-associated tumors, however, viral antigen expression is more restricted, and the aet

136 in lymphoid organs, as evidenced by limited viral antigen expression of rMd5/DeltavIL-8.

137 because of viral integration, persistence of viral antigen expression, inadequate HBV-specific immune

138 cyte and natural killer cell activation, and viral antigen expression.

139 d with the nuclear translocation of IRF3 and viral antigen expression.

140 na ganglion cell neurons; however, NS-gEnull viral antigens failed to reach the optic nerve, which in

141 inding and membrane fusion, and is the major viral antigen for antibody neutralization.

142 by higher cell-mediated immune responses to viral antigens for at least 17 weeks after SIV challenge

143 es provides the unique opportunity to target viral antigens for GBM therapy.

144 to provide a reliable source of standardized viral antigens for serodiagnosis of the medically import

145 Viral antigen from demyelinating strains is detected ini

146 geted therapies to enforce the expression of viral antigen from quiescent HIV-1 genomes, and immunoth

147 By blocking viral antigens from entering the endoplasmic reticulum,

148 Viral antigens fused to gD induced T and B cell response

149 s (bNAb) that target a conserved region of a viral antigen hold significant therapeutic promise.

150 induced-dendritic cells loaded with the pp65 viral antigen (iDCpp65) exhibited a faster development a

151 l epitopes, derived from both early and late viral antigens, illustrating a far broader T-cell repert

152 ts has been our limited understanding of the viral antigens important for protective antibodies.

153 Viral pneumonia and immunolocalization of viral antigen in association with diffuse alveolar damag

154 to an MHC class I-restricted peptide from a viral antigen in human peripheral blood mononuclear cell

155 infiltration and higher amounts of pulmonary viral antigen in marmosets.

156 We identified viral antigen in multiple organ tissues where it was not

157 All 4 GCA-positive TAs contained viral antigen in skip areas, mostly in the adventitia an

158 relate with infectious virus but did reflect viral antigen in some tissues.

159 ion between the differential localization of viral antigen in spinal cord gray matter and that in whi

160 control animals, as well as the presence of viral antigen in the brain, eye, pancreas, thyroid, and

161 alities, and have little infectious virus or viral antigen in the brain.

162 e of infection and prolonged presentation of viral antigen in the draining lymph nodes (DLN) of the r

163 ing most strongly with wider distribution of viral antigen in the lungs, rather than with traditional

164 conferred increased mortality and spread of viral antigen in the mouse central nervous system compar

165 d isolate cross-dressed APCs able to present viral antigen in vitro.

166 nent meningoencephalitis and the presence of viral antigen in WNVKOU-infected mice.

167 ging over 50%) of CD4(+) T cells specific to viral antigens in adults who had never been infected.

168 Previously, we detected many viral antigens in AEC-IIs from the lung.

169 ole in the modulation of immune responses to viral antigens in chronic viral hepatitis.

170 ich may contribute to weak immunogenicity of viral antigens in chronically infected humans.

171 erative responses to HCV peptide and control viral antigens in direct ex vivo assays.

172 s, and their reactivity to self-antigens and viral antigens in healthy subjects and patients with MS.

173 While viral antigens in human papillomavirus (HPV)-related oro

174 onstrations of NK cell memory of viruses and viral antigens in mice and primates.

175 Lipid-bilayer presentation of viral antigens in Nanodiscs is a new platform for evalua

176 The role of tumor-associated viral antigens in NPC renders it an appealing candidate

177 igen-specific T-cell responses toward common viral antigens in order to investigate defects in cellul

178 herefore, the direct detection of SARS-CoV-2 viral antigens in patient samples could also be used for

179 tive detection of IgG antibodies to multiple viral antigens in patient serum samples with detection l

180 alysis of the spatiotemporal distribution of viral antigens in the CNS of monkeys revealed a prominen

181 eroxynitrite production, is colocalized with viral antigens in the hearts of infected mice but not co

182 ulators of T-cell immunity against tumor and viral antigens in vitro than are monocyte-derived DCs (m

183 and whether the large amounts of circulating viral antigens inactivate the transferred T cells or lea

184 In this study, we inserted viral antigens into the C-terminal domain of gD and expr

185 ion is attenuated in mTEC cultures; however, viral antigen is detected predominantly in ciliated cell

186 ver, in HIV-infected individuals the load of viral antigen is not the limiting factor for the restora

187 ete clearance of the infection and even when viral antigen is undetectable by the most sensitive meth

188 However, exchange of archived viral antigens is mediated only by BatF3-dependent migra

189 increased viral load correlated with higher viral antigen levels in the bronchiolar epithelium and g

190 rred cells are able to expand in response to viral antigen, limit viral replication, and prevent prog

191 catalytic inhibitors or inhibition via tumor viral antigens, limited studies suggest that PP2A is a p

192 olor) with FeLV and quantitated proviral and viral antigen loads.

193 to white matter of the spinal cord, whereas viral antigen localization of nondemyelinating strains i

194 Viral antigen localized primarily to infected alveolar m

195 Viral antigen localizes in trophoblast and endothelial c

196 Persistent high levels of viral antigens may contribute to immune exhaustion.

197 ction is higher) or planned vaccination with viral antigens may enhance disease control.

198 oster immunizations or delivering additional viral antigens may not necessarily improve vaccine effic

199 cancer vaccine clinical trial based on a non-viral antigen, MUC1, in healthy individuals at-risk for

200 showed adventitial inflammation adjacent to viral antigen; no inflammation was seen in normal TAs.

201 Candidate "universal" vaccines targeting the viral antigens nucleoprotein (NP) and matrix 2 (M2), whi

202 Instead, the most protective mAbs bound viral antigen on the cell surface with high avidity and

203 As the sole viral antigen on the HIV-1 virion surface, Env is both t

204 However, the lack of expression of viral antigens on latently infected cells makes them dif

205 phene-oxide (rGO), and immobilizing specific viral antigens on the rGO nanoflakes.

206 aired T-cell recognition of tumor-associated viral antigens or their presenting HLA alleles.

207 7 of these cases were positive for influenza viral antigens or viral RNA, including four from the pre

208 ecise investigation of Trm recognizing novel viral antigens over time.

209 LMP1 and/or p24 compared with cases lacking viral antigens (P < .001) has important clinical implica

210 umans have preexisting immunity to influenza viral antigens, particularly antibodies to the HA and NA

211 We apply T-Scan to discover new viral antigens, perform high-resolution mapping of TCR s

212 ility of a host to prime naive T cells, that viral antigens persist in the infected host well beyond

213 Consistent with published data showing that viral antigen persistence impacts the function of circul

214 expression was increased and there were more viral antigen-positive cells and immune inflammatory cel

215 We focused on AEC-IIs as viral antigen-positive cells and on monocytes/macrophage

216 Wild-type mice had fewer viral antigen-positive cells with greater inflammation i

217 jasplakinolide results in reduced numbers of viral antigen-positive cells.

218 f infectious virus that we detected (PFU per viral antigen-positive neuron) was similar to that detec

219 ppressed control mice, replicating-virus-and viral-antigen-positive cells were not detected in the in

220 immunodeficiency virus, type 1 Nef disrupts viral antigen presentation and promotes viral immune eva

221 Finally, direct measurement of viral antigen presentation demonstrated an increase in C

222 These findings illustrate how endogenous viral antigen presentation during persistent viral infec

223 ly, most of the herpesviruses interfere with viral antigen presentation to cytotoxic T lymphocytes (C

224 ization strategy with DermaVir that improves viral antigen presentation using dendritic cells (DC).

225 Recognition of viral antigen presented by MHC molecules is crucial for

226 mmune response to HBV through alterations in viral antigen processing.

227 hus, these data demonstrate that circulating viral antigen produced during chronic infection can serv

228 Since new waves of viral antigen production could be induced with each boos

229 subsequent exposure to VOR, and to increase viral antigen production, this synergistic effect is dir

230 ion of cell-associated HIV RNA expression or viral antigen production.

231 receptor TLR3 in promoting cross-priming of viral antigens provide new insights into the mechanisms

232 Astrocytic cells positive for viral antigen provided support for an HHV-6-specific tro

233 whether viral antigens are necessary, or how viral antigens reach the stroma.

234 gle-cell transcriptomic analysis of >100,000 viral antigen-reactive CD4(+) T cells from 40 COVID-19 p

235 nors and identified rare (<0.001% frequency) viral-antigen-reactive TCRs.

236 Importantly, differential endogenous viral antigen recognition by CMV-specific CD8(+) T cells

237 he cell types that become infected or access viral antigens remains incompletely understood.

238 s I expression, or the expression of certain viral antigens, resulting in the elimination of affected

239 lls, whereas T cells specific for a non-self-viral antigen retained a CD44(low) naive phenotype.

240 ads to viral replication, with expression of viral antigens, RNA replication, and release of viral pa

241 rus vaccines (MVVs) or (2) isolating subunit viral antigen(s) to create individual antigen vaccines (

242 ese mutations are distinctly unlike self and viral antigens, signifying novel groups of potentially h

243 BP9 had increased AC accumulation, defective viral antigen-specific CD8+ T cell activation, enhanced

244 Viral antigen-specific ELISAs, qRT-PCR and TCID50 infect

245 Adoptive transfer of viral antigen-specific memory T cells can reconstitute a

246 cytokine staining was used to determine the viral antigen specificity and expression levels of vario

247 s generally inefficient, and the quantity of viral antigen strongly influenced CD8 T-cell antiviral f

248 e populations with infectivity, HCV RNA, and viral antigens suggests that infectious particles are li

249 of DNGR-1 to regulate cross-presentation of viral antigens suggests that this form of regulation of

250 but occur most visibly at times of prolonged viral antigen suppression by antiretroviral combination

251 reversible state of dormancy, with decreased viral antigen synthesis and increased therapeutic resist

252 EYFP(+) cells amass in areas associated with viral antigens, take on an activated morphology, and pro

253 HepG2/NTCP cells released more viral antigens than HepG2 cells after HBV genome deliver

254 higher antibody responses against the three viral antigens than those induced by the mixed vaccine.

255 vidence suggests that there may be depots of viral antigen that persist in draining lymph nodes (DLNs

256 We sought to engineer a viral antigen that provides greater protection than curr

257 racterization of these antibodies with their viral antigens that defines a few sites of vulnerability

258 pathic, and it is the immune response to the viral antigens that is thought to be responsible for hep

259 identify the immunogenic sites of a dominant viral antigen-the pentameric complex.

260 -like protein, m157, which is the only known viral antigen to date capable of engaging both activatin

261 epitopes, as well as direct presentation of viral antigen to Epstein-Barr virus-specific CD8+ T cell

262 RDCs then transport the viral antigen to the LNs draining the site of infection,

263 bservation suggests that the localization of viral antigen to white matter during the acute stage of

264 cells in chimeric mice efficiently presented viral antigen to wild-type T cells.

265 eic T cell responses and in cross-presenting viral antigens to CD8 T cells.

266 rter by HCMV US6 impairs the presentation of viral antigens to cytotoxic T lymphocytes.

267 cells in lymph nodes or the presentation of viral antigens to T cells to initiate an immune response

268 autophagy can be used to deliver endogenous viral antigens to the MHC class II loading compartment,

269 , and exclusively contained PCs specific for viral antigens to which the subjects had not been expose

270 and genes involved in cellular responses to viral antigens, together with complement inhibitory mole

271 up to 90-fold and maximizes the responses to viral antigens, tumour-associated antigens, oncofetal an

272 ing mouse brain (SMB) has been the source of viral antigens used in the assay.

273 nal analysis of antibody titers specific for viral antigens (vaccinia, measles, mumps, rubella, varic

274 Viral antigen was detected as early as 5 days postinfect

275 guinea pigs developed seroconversion and the viral antigen was detected in lungs of animals by immuno

276 Mumps viral antigen was detected in parotid glands by immunohi

277 Viral antigen was detected in small intestinal epithelia

278 hy was observed in the small intestines, and viral antigen was detected in villous enterocytes of the

279 ted in the lungs on day 2 postchallenge, and viral antigen was detected, by immunostaining, in the ep

280 Animals were viremic and viral antigen was first observed in multiple organs by d

281 ron and tumor necrosis factor in response to viral antigen was higher in settings where more severe d

282 caques died; immunohistochemical evidence of viral antigen was present in the brain and central nervo

283 Viral antigen was sufficient for PD-1 upregulation, but

284 Viral antigen was undetectable in the lungs on challenge

285 Viral antigen was widely detectable throughout the pulmo

286 Antibody responses to 646 viral antigens were assessed in 42 patients with T1D and

287 Viral antigens were detected in nasal turbinate, trachea

288 Previously, we reported that many viral antigens were detected in type II alveolar epithel

289 alternative 'biomimetic' technology; whereby viral antigens were formulated around a polymeric shell

290 Viral antigens were identified by an immunoconversion as

291 To alter the microenvironment and abundance, viral antigens were introduced as purified recombinant p

292 Viral antigens were localised to glial cells and neurons

293 Viral antigens were localized to ciliated respiratory ep

294 s, CD8(+) T cell responses to immunodominant viral antigens were oligoclonal, highly skewed, and exhi

295 OD of the negative control when reacted with viral antigen, were higher in CSF specimens (median, 14.

296 ce boostable functional antibodies against a viral antigen when administered with a needle-free devic

297 ties to secrete interleukin-2 in response to viral antigen, while secretion of gamma interferon (IFN-

298 on self-assembling nanoparticles of trimeric viral antigens, with SARS-CoV-2 spike-LuS nanoparticles

299 ostmortem tissue samples show high levels of viral antigen within the respiratory endothelium, but it

300 polyinosinic-polycytidylic acid (poly(I:C), viral antigen) would decrease P-gp and BCRP in the human