ライフサイエンスコーパス: escape variant

1 ss-reactive immune responses against the Gag escape variant.

2 r function, driving the selection of a viral escape variant.

3 n the S protein, known as a potential immune escape variant.

4 wn that SARS-CoV-2 BA.1 omicron is an immune escape variant.

5 against infection with the DBN3a sofosbuvir escape variant.

6 ight retain protective activity even against escape variants.

7 key contributor for the selection of immune escape variants.

8 y, resulting in the continuous generation of escape variants.

9 chanisms affects the rate of invasion of IAV escape variants.

10 vent the emergence of cytotoxic T-lymphocyte escape variants.

11 o immune editing and recognize newly arising escape variants.

12 mother-to-child transmission of CD8+ T cell escape variants.

13 a-mIgG), can select different populations of escape variants.

14 is is not due to the evolution of new immune escape variants.

15 gh functional avidity can rapidly select for escape variants.

16 es of pulmonary immunity in selection of CTL escape variants.

17 tumor growth but not the later appearance of escape variants.

18 for years without inducing detectable viral escape variants.

19 emdesivir significantly reduced emergence of escape variants.

20 able to clear HDV because of the presence of escape variants.

21 ting vaccine efficacy and detecting emerging escape variants.

22 e can eradicate melanomas containing antigen escape variants.

23 y syndrome coronavirus 2 (SARS-CoV-2) immune-escape variants.

24 he therapeutic selective pressure for immune escape variants.

25 y viral evolution and the emergence of novel escape variants.

26 sate for the replicative fitness loss of IAV escape variants.

27 branches of the immune system may eliminate escape variants.

28 increasing the chances of neutralizing viral escape variants.

29 V-2 variants, as well as 20 potential future escape variants.

30 on of functional SARS-CoV-2 S neutralization escape variants.

31 rs and help protect against the emergence of escape variants.

32 , hence, a greater efficiency in controlling escape variants.

33 cantly reduced the emergence of immunoedited escape variants.

34 bs by preventing the emergence of bNAb viral escape variants.

35 as well as those that do rapidly select for escape variants.

36 to prevent the emergence of fully functional escape variants.

37 ork that could provide protection from virus-escape variants.

38 ich was consistent with immune selection for escape variants.

39 which give rise to drug-resistant and immune escape variants.

40 ons of residues that are mutated in antibody escape variants.

41 termined targets and are prone to select for escape variants.

42 ion without the emergence of S1P-independent escape variants.

43 h PSC-RANTES were analyzed for possible drug escape variants.

44 e animal to mount secondary responses to the escaped variants.

45 over several weeks without the emergence of escape variants able to use other cellular proteases for

46 n at position 6 (L6M), which arises as a CTL escape variant after primary infection but is sufficient

47 ease and the emergence of antigen-loss tumor escape variants after treatment demonstrate the need to

48 sis of representative variants revealed that escape variants also induced NAbs within a few weeks of

49 dition infection assay further validated the escape variant and showed that all monoclonal antibodies

50 oceeded by neutralizing Ab production to the escape variant and subsequent escape.

51 the targeted cells without the appearance of escape variants and allowed efficient and simultaneous c

52 ral pathogenesis and the emergence of immune escape variants and for design of vaccine strategies.

53 not susceptible to classic CD4 binding site escape variants and maintained full viral suppression in

54 n anomalous random walk determined by future escape variants and results in variant trajectories that

55 However, antigen-loss tumor escape variants and the absence of currently targeted an

56 aid in the prediction of potential antigenic escape variants and the selection of future vaccine cand

57 rom HIV-transmitted/founder (T/F) and immune escape variants and their mutants involving the N262 gly

58 ted in the rapid selection of neutralization escape variants and treatment failure in mice.

59 enotype 1-7 prototype isolates and resistant escape variants, and investigated the effects of pre-exi

60 d in genotype 1 glecaprevir and voxilaprevir escape variants, and pre-existing A156T facilitated geno

61 c T helper cells, the emergence of antigenic escape variants, and the expression of an envelope compl

62 nvergent microevolution, appear to be immune-escape variants, and were evolutionarily constrained at

63 addition to the emergence of HVR-1 antibody escape variants are involved in maintaining viral persis

64 Tumor escape variants are likely to emerge after treatment wit

65 receptors and thus still be immunogenic when escape variants are passed to individuals expressing the

66 n experiments demonstrate that the very rare escape variants are rendered almost non-infectious.

67 plex provide a strong basis for why some CTL escape variants are selected, our results also show that

68 Patterns of immune escape variants are similar in HIV type 1-infected human

69 ell responses that do not rapidly select for escape variants are unable to control viral replication

70 The results demonstrate that neutralization-escape variants arise periodically in HIV-1-infected lon

71 cies can differ in the ease with which viral escape variants arise.

72 Our findings portend continued emergence of escape variants as SARS-CoV-2 adapts to humans.

73 8+ T cell responses against predicted immune escape variants, as well as subdominant conserved HIV ep

74 tions for predicting the selection of immune escape variants at a population level.

75 eradicate virus did not reflect selection of escape variants because the gag epitope remained unmutat

76 initially cornered low-replicative-capacity escape variants, but with insufficient avidity to preven

77 g to HLA-B57, suggesting that sensing of CTL escape variants by NK cells can contribute to the protec

78 his antigenic redundancy may prevent vaccine escape variants by recombinational loss, which is freque

79 S hotspot for genotype 1-4, but not 5 and 6, escape variants by resistance profiling using PIs grazop

80 tralization by generating and characterizing escape variants by whole-genome sequencing.

81 preclinical models of glioblastoma, antigen escape variants can lead to tumor recurrence after treat

82 Host selection of viral CD8 escape variants can subvert vaccine-conferred immunity.

83 None of the escape variants caused breakthrough replication in LTNPs

84 favored the undetected spread of the antigen-escape variant compared to the rest of Italy.

85 ian reservoir host, during which time immune escape variants continually arise in part because of var

86 These findings indicate that sofosbuvir escape variants could compromise the effectiveness of nu

87 NGS heterogeneity between the T/F and immune escape variants defined a range of NGS that we further p

88 iation of therapy, and then finally to a new escape variant during continued therapy.

89 t(28-35) SL8, which reproducibly selects for escape variants during acute infection, and Gag(181-189)

90 rapy and for the selection of neutralization escape variants during hE16 treatment.

91 T-lymphocyte responses select for new viral escape variants during the acute phase of infection.

92 ransmitted/founder virus(es) (acute ARTi) or escape variants (early ARTi) were tested for sensitivity

93 system cannot control tumor growth, but how escape variants emerge during immunotherapy remains poor

94 nfection-induced antibodies suggests that if escape variants emerge they may be readily selected for

95 es exert selective pressure on the virus but escape variants emerge within a short period of time.

96 Escape variants emerged rapidly in the group 1 vaccinees

97 An in-depth study of escape variants emerging under host immune pressure duri

98 Our results suggest that some escape variant epitopes evolving in infected individuals

99 e parental West Nile virus, a neutralization escape variant failed to cause lethal encephalitis (at h

100 hree were on-drug relapses, with the CD19(-) escape variant first detected after only 2 treatment cou

101 Therefore, somatic escape variants from a deleterious germline variant are

102 We also selected antigenic escape variants from human viruses treated with convales

103 Engineered escape variants had high levels of fitness.

104 CTLs in viral clearance and selection of CTL escape variants have been evaluated.

105 ical peptide and KIR binding residues of the escape variants have selectively converged to resemble t

106 ls significantly faster (P = 0.004) and that escape variants have significantly higher fitness costs

107 HBV) genome able to explain an immunological escape variant.HBV genome has a very compact coding orga

108 inhibited NA activity but did not result in escape variants, highlighting its suitability for develo

109 us epitopes tested represented potential CTL escape variants; however, in most cases strong responses

110 immunodeficiency virus type 1 generate viral escape variants; however, the mechanisms of escape are n

111 With the emergence of SARS-CoV-2 immune escape variants, humoral immunity is being challenged, a

112 Selection of immune escape variants impairs the ability of the immune system

113 ns that may allow the anticipation of immune escape variants.IMPORTANCE The Env protein of HIV is hig

114 g oligoclonality resulted in an LCMV epitope escape variant in vivo resembling the natural Lassa viru

115 uble mutant (E1-K61T E2-D59N) neutralization escape variant in WT mice.

116 among S. flexneri that may generate vaccine escape variants in <6 months.

117 t an example of shifting immune responses to escape variants in a patient with sequential metastases

118 Here, we describe the evolution of antigenic escape variants in a rhesus macaque that developed unusu

119 The occurrence of viral escape variants in an N6-LS-monotreated animal, however,

120 CD8(+) T lymphocytes (CD8-TL) select viral escape variants in both human immunodeficiency virus and

121 (Nef(165-173)IW9) typically select for viral escape variants in early SIV(mac)239 infection.

122 Maintenance of such escape variants in human populations could pose an obsta

123 Abs on SARS-CoV-2 can lead to development of escape variants in immunocompromised patients.

124 r could function to prevent the emergence of escape variants in infected hosts.

125 tecting antibiotic resistance and diagnostic escape variants in Neisseria gonorrhoeae, a pathogen ass

126 tance and the potential emergence of vaccine-escape variants in Plasmodium falciparum threaten progre

127 hat have the potential to rapidly select for escape variants in the early phase of infection are need

128 We investigated the patterns of T cell escape variants in the replication-competent reservoir o

129 es and limited cytotoxic T lymphocyte immune escape variants in the reservoir.

130 ocument transmission of viruses encoding CTL escape variants in this dominant Gag epitope that no lon

131 ancestral SARS-CoV-2 strains, others induced escape variants in vivo or lost neutralizing activity ag

132 tive inhibitor of NA activity selected pH1N1 escape variants in vivo.

133 ng disclosed highly aberrant CTCs as therapy-escaping variants in breast cancer.

134 ast to influenza viruses for which 4-GU-DANA escape variants include hemagglutinin mutants with decre

135 city CD8(+) T cells led to the appearance of escape variants, indicating that broader epitope specifi

136 ulation, and durability of immune responses, escape variants initially grow exponentially, but lose t

137 contrast to the relatively high frequency of escape variants initially observed, the subsequent emerg

138 also suggested that the number of potential escape variants is limited by previous exposure to seaso

139 ng the breadth of antiviral immunity against escape variants is through the generation of memory T ce

140 An escape variant, J178V, was generated in vitro, and the l

141 ation, preemptive immunization against these escape variants led to the generation of secondary CD8(+

142 bility of emergence of S1P-independent viral escape variants make S1P-mediated GPC processing by pept

143 Mother-to-child transmission of CD8+ T cell escape variants may particularly affect CD8+ T cell reco

144 Finally, infection with CD8 T cell escape variants may result in a compensatory increase in

145 To avoid severe side effects and tumor escape variants observed for conventional CAR-T cells ap

146 ve described previously the generation of an escape variant of human immunodeficiency virus type 1 (H

147 ajority of the subjects targeted the G(357)S escape variant of the Gag(349-359) epitope, while the wi

148 a demonstrate that de novo responses against escape variants of CD8(+) T-cell epitopes can be generat

149 e fight against COVID-19 continues as immune escape variants of concern such as Delta and Omicron eme

150 Neutralization-escape variants of human immunodeficiency virus type 1 (

151 y tract is a suitable site for generation of escape variants of influenza virus selected by CTL in vi

152 ve antibodies, especially when facing immune escape variants of SARS-CoV-2.

153 The emergence of immune-escape variants of severe acute respiratory syndrome cor

154 body was mapped by sequencing neutralization escape variants of the virus.

155 Escape variants of the ZIKV MR766 strain to a potently n

156 HIV-infected cells and recognized all common escape variants of this epitope.

157 mutation, which leads to the generation of 'escape' variants of HCV that persist as a quasi-species

158 However, antigen-negative escape variants often cause disease relapse, necessitati

159 f emergence and the biological impact of CTL escape variants on the clinical outcome of influenza pne

160 , and older immune responses wane, such that escape variants only enjoy a growth advantage for a limi

161 nabling rapid response strategies to address escape variants or lessen escape vulnerabilities.

162 accine effectiveness (eg, waning immunity or escape variants), or increase social interactions among

163 We investigated to what extent reactivity to escape variant peptides in standard enzyme-linked immuno

164 However, recognition of escape variant peptides was commonly observed in both EC

165 e (CTL) selection of hepatitis C virus (HCV) escape variants plays a role in HCV persistence.

166 Escape variant populations derived by propagating suscep

167 While other data-driven viral escape variant predictor tools have shown promise in pre

168 including two that do not rapidly select for escape variants, predominated during early m3KODeltanef

169 he ability of HIV-1 to rapidly establish CTL escape variants presents major hurdles toward this goal.

170 TL-targeted epitope changed from an apparent escape variant prior to the initiation of therapy, to th

171 icts likely antigenic profiles of successful escape variants prior to their emergence.

172 An understanding of ZM1 and other escape variants provides insight into the effects of thi

173 sidues frequently mutated in clinical immune escape variants, provides a molecular explanation for wh

174 ssortment, zoonotic transmission, and immune escape variants, providing crucial insights for assessin

175 If an escape variant reaches fixation in the population, the e

176 We conclude that selection of viral CTL escape variants reflects coordinate action between the t

177 These CTL escape variants remain stable without reversion in the a

178 conserved HIV epitopes and predicted immune escape variants required to control HIV replication and

179 Selection of an escape variant revealed that NS5A is directly or indirec

180 studied, although the spectrum of viral CTL escape variants selected varied profoundly.

181 All escape variants showed evidence of mild clinical attenua

182 Three out four huTRIM5alpha escape variants showed resistance to all primate TRIM5al

183 uent copy-number variations including immune escape variants such as high-level amplifications of the

184 ame donor were able to neutralize some VRC01 escape variants, suggesting that CD4bs antibodies contin

185 A common acute escape variant, T170I, unexpectedly and uniquely degrade

186 Tumor escape variants (TEV) recovered from the lungs of CTL-tr

187 Interestingly, the one escape variant that was detected proved to be a CTL anta

188 he patients were infected with potential CTL escape variants that contained nonimmunogenic and noncro

189 This implies that many pathogen epitope escape variants that could manifest as single amino-acid

190 riving the development of more complex viral escape variants that disrupt antigen presentation.

191 ineered receptors, enabling the formation of escape variants that elude CAR T cell targeting.

192 es not appear to be a result of selection of escape variants that lack the MAb 2H1 epitope.

193 de an early warning system of neutralization escape variants that may impact transmission or the effe

194 ion unmasked the occurence of oncogenic KRAS escape variants that were resistant to Cas9-cleavage.

195 vaccination provides some protection against escape variants, the corresponding reduction in prevalen

196 I (MHC-I) gene restricts the advantage of an escape variant to only a small fraction of the human pop

197 dy (aNAB) in selective transmission of HIV-1 escape variants to infants.

198 S-CoV-2 could increase selection for vaccine-escape variants, ultimately undermining vaccine effectiv

199 the emergence of distinct repertoires of HA escape variants under neutralizing antibody pressure.

200 These data suggest that TW10 escape variants undergo a postentry block that is partia

201 to capture a wild-type and a neutralization escape variant virus equally well.

202 ly reasonable parameters, the invasion of an escape variant virus will be slow, with a timescale of a

203 MAb resistance, we engineered neutralization escape variant viruses (E1-K61T, E2-D59N, and the double

204 ngly, we found evidence for the selection of escape variant viruses by CTL specific for Nef(159-167)

205 These so-called "CTL escape variant viruses" are commonly selected during per

206 d to select single and double neutralization escape variant viruses, and determination of the amino a

207 gnition of cells infected with corresponding escape variant viruses.

208 developed clinical disease, and harbored CTL escape variant viruses.

209 otecting from the selective outgrowth of CTL escape variant viruses.

210 Transmission of escape variants was confirmed.

211 e to TL-3, a panel of chronological in vitro escape variants was generated.

212 Thus, a less-restricted repertoire of escape variants was observed in mice with an intact perf

213 served, the subsequent emergence rate of CTL escape variants was very low.

214 Based on selection of escape variants, we show that D1-8 targets a novel epito

215 alence of subtypes/genotypes and drug/immune-escape variants were characterized by comparing recently

216 with control of viremia, and neutralization escape variants were detected concurrently with the gene

217 Several CD8+ T cell escape variants were detected in maternal plasma.

218 Neutralization escape variants were discovered shortly thereafter, and,

219 Emerging escape variants were generally resistant to the related

220 Several HIV-1 CD8(+) T cell escape variants were identified within maternal plasma v

221 Escape variants were observed at different time points w

222 e expression efficiency, as well as antibody escape variants, were also identified.

223 iding broad neutralization and prevention of escape variants when combined with other nAbs that targe

224 rtoire that fails to recognize specific KF11 escape variants which frequently arise in clade C-infect

225 ressure from pathogen decoys selects for IgA escape variants which, in turn, selects for FcalphaRI va

226 ns, has been complicated by the emergence of escape variants, which has been seen for pathogens such

227 ,806 SARS-CoV-2 sequences predicted emerging escape variants, which were also effectively neutralized

228 dren exhibited a robust response to the TW10 escape variant while recognizing the wild-type epitope w

229 can optimize an antibody to target multiple escape variants, while simultaneously enriching potency.

230 3a to sofosbuvir led to identification of an escape variant with substitutions in NS5B, including the

231 pe protein which likely allowed selection of escape variants with a conformational switch in the V2 d

232 Escape variants with alterations in the lgtG repeat trac

233 llowed by viral rebound and the emergence of escape variants with lower replicative capacity.

234 nal response, enabled the rational design of escape variants with minimal disruption to cell tropism

235 of mouse hepatitis virus, which exhibit CTL escape variants with mutations in a single epitope from

236 Escape variants with such extended CP fail to be transmi

237 This coincided with the emergence of an escape variant within the Tat epitope and an additional

238 ogous viruses revealed the absence of immune escape variants within five of the six epitopes.