ライフサイエンスコーパス: viral antigen

1 esentation of the intracellular reservoir of viral antigen.

2 ction have reported systemically distributed viral antigen.

3 liferation that correlated with abundance of viral antigen.

4 al for both sampling and presenting residual viral antigen.

5 a homologous and potentially cross-reactive viral antigen.

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

7 e new neutralizing antibodies to the mutated viral antigen.

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

9 AT1 in bystander cells staining negative for viral antigen.

10 of viral infections and tumors that express viral antigens.

11 timulates a state of unresponsiveness toward viral antigens.

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

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

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

15 machinery for MHC II presentation of herpes viral antigens.

16 ies and by tissue colocalization of distinct viral antigens.

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

18 yielded >300 unique antibodies against H5N1 viral antigens.

19 ne effectors that mediate rapid responses to viral antigens.

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

21 n a second lipid membrane containing several viral antigens.

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

23 since they lack expression of immunodominant viral antigens.

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

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

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

27 nerated especially strong responses to lytic viral antigens.

28 unotherapy targeted against tumor-associated viral antigens.

29 mmatory responses in the absence of virus or viral antigens.

30 -lymphocyte (CTL) responses in vitro against viral antigens.

31 lls in humans and modify immune responses to viral antigens.

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

33 duration, implying prolonged presentation of viral antigens.

34 for oral HPV infection or seroreactivity to viral antigens.

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

36 ncer germline antigen, rather than canonical viral antigens.

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

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

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

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

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

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

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

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

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

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

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

48 Viral antigen and nucleic acid were detected in bronchio

49 Viral antigen and RNA staining decreased in targeted and

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

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

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

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

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

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

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

57 naling defects associated with expression of viral antigens and HIV-1 replication in the brain.

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

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

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

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

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

63 oad specificity for other stimuli, including viral antigens and third-party alloantigens.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 Localization of viral antigens at different survival times (66-96 hours)

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

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

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

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

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

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

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

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

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

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

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

91 Distribution of viral antigens by immunohistochemistry correlated with t

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

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

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

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

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

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

98 Vaccination with viral antigens combined with adjuvant correlated with th

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

100 e H5N1 isolates in that infectious virus and viral antigen could also be detected in muscle and brain

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

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

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

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

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

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

107 lammatory mediators following recognition of viral antigen displaying cells.

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

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

110 Viral antigen distribution in the respiratory tree, howe

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

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

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

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

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

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

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

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

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

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

121 8+ CTL response was found to be specific for viral antigens expressed during the immediate early and

122 The majority of viral antigen-expressing cells were CD4(+) T lymphocytes

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

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

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

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

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

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

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

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

131 ver, the preparation of cell culture-derived viral antigen for these tests is laborious and variable

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

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

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

135 Viral antigen from demyelinating strains is detected ini

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

137 By blocking viral antigens from entering the endoplasmic reticulum,

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

139 rus type 1, but neither the viral genome nor viral antigens have been demonstrated in pathologic lesi

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

141 Kidney infection as determined by viral antigen ICC predominantly involved the tubular epi

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

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

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

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

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

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

148 e Ab suppressed virus recrudescence, reduced viral antigen in most cell types except oligodendroglia,

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

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

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

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

153 D8(+) cells exhibited much reduced levels of viral antigen in the brain as measured by immunohistoche

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

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

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

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

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

159 y depleted of CD4 T cells had high levels of viral antigen in tissues earlier (days 50 to 70) than va

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

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

162 zed readily by the immune system and present viral antigens in a more authentic conformation than oth

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

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

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

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

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

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

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

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

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

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

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

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

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

176 the immune response can be targeted against viral antigens in those patients infected with hepatitis

177 y clearing the infection, were found to have viral antigens in tissues later (day 120 to 150 post-int

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

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

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

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

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

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

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

185 n their Perspective, at least in the case of viral antigens, it seems that other dendritic cell subse

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

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

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

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

190 Viral antigen localized primarily to infected alveolar m

191 Viral antigen localizes in trophoblast and endothelial c

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

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

194 sence of antibodies specific to at least two viral antigens, mostly NS3 and E2.

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

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

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

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

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

200 7 of these cases were positive for influenza viral antigens or viral RNA, including four from the pre

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

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

203 to testing an antibody response to a single viral antigen per reaction, thus necessitating a panel o

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

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

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

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

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

209 out the presence of macrophages, T cells, or viral antigen-positive cells.

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

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

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

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

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

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

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

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

218 lymphoblastoid cell lines (EBV-LCL) as our (viral) antigen-presenting cells and overexpressed the No

219 stochemistry for EBV or HHV-8 antigen showed viral antigen primarily in airway epithelial cells.

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

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

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

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

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

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

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

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

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

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

230 significance of the discrepant expression of viral antigens remains uncertain.

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

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

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

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

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

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

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

238 be a target for adoptive immunotherapy with viral antigen-specific T cells.

239 tigen-presenting cells; adoptive transfer of viral antigen-specific T cells; and targeting AFP-expres

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

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

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

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

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

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

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

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

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

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

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

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

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

253 icient mice depleted of CD8 T cells had high viral antigen titers in tissues following intraperitonea

254 umbed to subcutaneous infection and had high viral antigen titers in tissues, whereas mice deficient

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

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

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

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

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

260 s cell-derived or CD8alpha(+) DCs, presented viral antigens to CD4(+) T cells and induced IFNgamma se

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

262 R) is a critical step in the presentation of viral antigens to CD8+ T cells.

263 r by vaccination may need to target multiple viral antigens to completely restore immunologic control

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

265 future EBV vaccine strategies should target viral antigens to DCs.

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

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

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

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

270 were similar regardless of the strain of WN viral antigen used, and only minimal cross-reactivity wa

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

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

273 Viral antigen was detected as early as 5 days postinfect

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

275 Mumps viral antigen was detected in parotid glands by immunohi

276 Viral antigen was detected in small intestinal epithelia

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

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

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

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

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

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

283 Viral antigen was undetectable in the lungs on challenge

284 Viral antigen was widely detectable throughout the pulmo

285 using either allogeneic stimulator cells or viral antigens, we found that coexpression of activation

286 Replicating virus and viral antigen were detected in the injected eyes, periph

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

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

289 Viral antigens were identified by an immunoconversion as

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

291 Viral antigens were localised to glial cells and neurons

292 Viral antigens were localized to ciliated respiratory ep

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

294 f CD4(+)- and CD8(+)-T-cell responses to all viral antigens were similar, with only minor differences

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 In addition, colocalization of viral antigen with infiltrating leukocytes in the iris a

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